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"Lipid"

Correspondence

Correspondence to editorial on “A New Lens on Ferroptosis in Liver Disease: Near-Infrared Fluorescent Probe of Lipid Peroxidation-Driven Microenvironmental Remodeling” and “Mapping Lipid Droplet Viscosity: A Novel Tool for Spatiotemporal Ferroptosis”
Taeeung Kim, Le Bich Hang Pham, Jeeyeon Lee, Keon Wook Kang
Received January 20, 2026  Accepted February 2, 2026  Published online February 5, 2026  
DOI: https://doi.org/10.3350/cmh.2026.0094    [Accepted]
  • 85 View
  • 9 Download

Editorial

A New Lens on Ferroptosis in Liver Disease: Near-Infrared Fluorescent Probe of Lipid Peroxidation–Driven Microenvironmental Remodeling. Editorial on “Novel Near-Infrared Probe for Monitoring Lipid Peroxidation-Mediated Viscosity Change in Ferroptotic Hepatocytes”
Yunseo Bong, Wonhyo Seo
Received January 2, 2026  Accepted January 17, 2026  Published online January 27, 2026  
DOI: https://doi.org/10.3350/cmh.2026.0003    [Accepted]
  • 157 View
  • 18 Download

Original Article

Novel near-infrared probe for monitoring lipid peroxidation-mediated viscosity change in ferroptotic hepatocytes video
Le Bich Hang Pham, Taeeung Kim, Seoyoung Kim, Yun Seok Kim, Jiyeon Kim, Kyeongseon Kim, Hyeonwoo Lim, Wan Seob Shim, Byoungmo Kim, So-Yeol Yoo, Jae-Young Lee, Murim Choi, Won Kim, Keon Wook Kang, Jeeyeon Lee
Clin Mol Hepatol 2026;32(1):318-338.
Published online November 17, 2025
DOI: https://doi.org/10.3350/cmh.2025.0779
Background/Aims
Ferroptosis, recently emerged as a new cell death modality characterized by iron-dependent peroxidation of lipids, has been explored in various diseases. However, detection of ferroptosis, particularly in chronic liver disease models, is hampered by the lack of universal ferroptosis markers and limited number of fluorescence sensors for in vivo ferroptosis.
Methods
In this study, we developed TTM-4 as a highly sensitive near-infrared (NIR) fluorescent probe to detect ferroptosis.
Results
TTM-4 exhibited turn-on fluorescence upon viscosity change, enabling visualization of lipid peroxidation (LPO) in ferroptotic hepatocytes and liver tissue samples with greater sensitivity than BODIPY 581/591 C11. Timelapse live-cell imaging of erastin-treated cells revealed real-time LPO dynamics involving cytosolic lipid droplets (cLDs), endoplasmic reticulum, and nuclear LDs in a chronological order. Further gene expression analysis of 216 liver tissue samples from the NCBI GEO database showed a significant increase in CIDEC concurrent with TTM-4 fluorescence during progression to metabolic dysfunction-associated steatotic hepatitis (MASH). TTM-4, with its low toxicity and turn-on NIR emission during ferroptosis, also enabled in vivo visualization of ferroptosis in liver injury and metabolic dysfunction-associated steatotic liver disease (MASLD) models.
Conclusions
Our findings suggest that TTM-4 enables monitoring of ferroptosis in MASLD and would aid in early MASH diagnosis.
  • 1,611 View
  • 174 Download

Letter to the Editor

Plasma lipidomic and fungal signatures predict early mortality in acute liver failure
Yu Ji Kim, Jong-Won Kim
Clin Mol Hepatol 2026;32(1):e21-e23.
Published online August 20, 2025
DOI: https://doi.org/10.3350/cmh.2025.0813
  • 2,267 View
  • 66 Download

Correspondence

Correspondence to editorial on “CD36 Promotes iron accumulation and dysfunction in CD8+ T cells via the p38-CEBPB-TfR1 axis in early-stage hepatocellular carcinoma”
Yifei Qin, Peng Lin, Huijie Bian, Zhi-Nan Chen, Jiao Wu
Clin Mol Hepatol 2026;32(1):e75-e78.
Published online April 28, 2025
DOI: https://doi.org/10.3350/cmh.2025.0402
  • 5,580 View
  • 49 Download

Research Letter

Lipidomic analysis of alcohol use disorder patients revealed the biomarkers for alcohol-related liver disease susceptibility
Dongyao Wang, Hongwei Zhang, Yuxiao Tang
Clin Mol Hepatol 2025;31(3):e259-e262.
Published online April 2, 2025
DOI: https://doi.org/10.3350/cmh.2025.0227

Citations

Citations to this article as recorded by  Crossref logo
  • Discovery of Bufalin as a Molecular Glue Degrader of NCAPG to Inhibit the Proliferation of Hepatoma Cells
    Chenghua Wu, Xiaobin Zhuo, Jianxin Yang, Yuxiao Tang, Weili Wang, Mengpu Wu, Gen Miao, Chenqi Li, Hui Shen, Jianxin Qian, Dongyao Wang
    Drug Development Research.2026;[Epub]     CrossRef
  • Targeting Annexin A2 to reactivate tumor-associated antigens presentation and relieve immune tolerance in liver cancer
    Yuxiao Tang, Jianxin Yang, Qicong Shen, Zelong Gao, Mengpu Wu, Chenghua Wu, Jicong Du, Min Li, Changquan Ling, Feng Lu, Yifeng Chai, Xin Dong, Jianxin Qian, Chenqi Li, Feng Xie, Zhenhong Guo, Hui Shen, Dongyao Wang
    Journal for ImmunoTherapy of Cancer.2025; 13(6): e011716.     CrossRef
  • 8,479 View
  • 98 Download
  • 1 Web of Science
  • Crossref

Original Article

CD36 promotes iron accumulation and dysfunction in CD8+ T cells via the p38-CEBPB-TfR1 axis in early-stage hepatocellular carcinoma
Yifei Qin, Fei Huo, Zhuan Feng, Jialu Hou, Yaxin Ding, Quancheng Wang, Yu Gui, Ziwei Yang, Jiali Yang, Gang Zhou, Ling Li, Jianli Jiang, Lingmin Kong, Shijie Wang, Gang Nan, Dingqiao Xu, Xiaohang Xie, Lijuan Wang, Qian He, Ruibin Yang, Peng Lin, Huijie Bian, Zhi-Nan Chen, Jiao Wu
Clin Mol Hepatol 2025;31(3):960-980.
Published online March 4, 2025
DOI: https://doi.org/10.3350/cmh.2024.0948
Background/Aims
The identification of factors that lead to CD8+ T cell dysfunction within the tumor microenvironment (TME) holds great promise for the development of innovative immunotherapies. However, the mechanisms underlying the exhausted phenotype of CD8+ T cells infiltrating early-stage hepatocellular carcinoma (HCC) tumors remain unclear.
Methods
Single-cell RNA sequencing was performed using a murine HCC model. Flow cytometry and additional experimental approaches were employed to investigate the mechanisms of CD8+ T cell exhaustion.
Results
CD8+ T cells infiltrating early-stage HCC exhibited a functionally exhausted phenotype, which escalated with HCC progression. At early stages of HCC, the TME was characterized by significant iron accumulation. Moreover, tumor-infiltrating CD8+ T cells in murine HCC exhibited higher levels of intracellular ferrous iron compared to splenic CD8+ T. This excessive iron led to increased lipid peroxide levels and impaired the effector function of CD8+ T cells. Mechanistically, CD36 upregulated the iron uptake protein transferrin receptor 1 (TfR1) by mediating the activation of oxidized low-density lipoprotein (oxLDL)-p38-CEBPB axis. Depletion of CD36 in CD8+ T cells inhibited the upregulation of TfR1 and the increase of iron levels. Furthermore, constitutively activated nuclear factor erythroid 2-related factor 2 (NRF2) effectively suppressed lipid peroxidation, thereby preserving the effector functions of intratumoral CD8+ T cells and ultimately inhibiting tumor growth.
Conclusions
Our findings reveal a previously unidentified mechanism mediated by CD36 that regulates the progressive dysfunction of CD8+ T cells in early HCC TME and provide a potential novel therapeutic approach to restore T cell function.

Citations

Citations to this article as recorded by  Crossref logo
  • Correspondence to editorial on “CD36 Promotes iron accumulation and dysfunction in CD8+ T cells via the p38-CEBPB-TfR1 axis in early-stage hepatocellular carcinoma”
    Yifei Qin, Peng Lin, Huijie Bian, Zhi-Nan Chen, Jiao Wu
    Clinical and Molecular Hepatology.2026; 32(1): e75.     CrossRef
  • The Role of Low CD36 Expression in the Development of Non-Small Cell Lung Cancer and Its Potential for Therapy
    Ran Wu, Xiaohong Xu, Danju Luo, Junhua Wu, Xiaona Chang, Chenggong Ma, Bo Huang, Jun Fan, Xiu Nie
    Cancers.2026; 18(2): 217.     CrossRef
  • Senescent fibroblasts drive CD8+ T cell dysfunction in colorectal cancer via CD36-mediated lipid transfer and peroxidation
    Mengxiao Ge, Shuangyi Sun, Wentong Chen, Zhenxiao Xu, Deyi Kang, Zeqin Wang, Yumeng Guo
    Journal of Translational Medicine.2026;[Epub]     CrossRef
  • Adjuvant cytokine-induced killer cell immunotherapy in hepatocellular carcinoma: real-world data and 9-year extended follow-up of a randomized controlled trial
    Hyunjae Shin, Youngsu Park, Byeong Geun Song, Won-Mook Choi, Hyung Joon Han, Youngwoo Lee, Tae-Jin Song, Jong-Eun Yeon, Young-Suk Lim, Moon Haeng Hur, Yun Bin Lee, Eun Ju Cho, Su Jong Yu, Yoon Jun Kim, Joon Hyeok Lee, Jung-Hwan Yoon, Jeong-Hoon Lee
    Cancer Immunology, Immunotherapy.2026;[Epub]     CrossRef
  • Dietary lipids synergistically enhance PAH bioavailability and intestinal toxicity: Mechanistic insights from a Caco-2 model
    Xiaofang Liu, Jie Zhu, Wanyi Zou, Li Liang, Jixian Zhang, Chaoting Wen, Youdong Li, Guoyan Liu, Xin Xu
    Food Bioscience.2026; 77: 108374.     CrossRef
  • Reprogrammed Lipid Metabolism as a Gatekeeper of Hepatocarcinogenesis: from Enzyme Regulation to Precision Therapy
    Luxi Yang, Jing Yang, Zhonghong Xiong, Jinsen Wei, Xiaojuan Jiang, Huili Ye, Yumin Li
    Current Oncology Reports.2026;[Epub]     CrossRef
  • The dual role of CD36 in cancer: from lipid metabolism to tumor microenvironment regulation
    Yixuan Yao, Yanyuan Fang, Bin Yuan, Jing Yang
    Molecular Biology Reports.2025;[Epub]     CrossRef
  • Oxidative stress in cancer: from tumor and microenvironment remodeling to therapeutic frontiers
    Xisong Liang, Jiadi Weng, Zhongyi You, Yang Wang, Jie Wen, Zhiwei Xia, Shaorong Huang, Peng Luo, Quan Cheng
    Molecular Cancer.2025;[Epub]     CrossRef
  • Targeting Ferroptosis Restores the Antiviral Activity of CD8+ T Cells During Chronic Hepatitis B Virus Infection
    Haohao Li, Su Xiao, Chenxin Huo, Shasha Yang, Jun Wang, Xinxing Lan, Menghua Li, Lizhi Shi, Li Zhuo, Jian Zhang, Huajun Zhao, Qiuju Han
    Cellular and Molecular Gastroenterology and Hepatology.2025; 19(12): 101612.     CrossRef
  • Targeting lipid metabolism to enhance cancer immunotherapy
    Dan Zhao, Lei Wu, Yongsheng Li
    Biochimica et Biophysica Acta (BBA) - Reviews on Cancer.2025; 1880(5): 189416.     CrossRef
  • Establishment of an anaplastic stratification signature for gastric cancer based on diverse regulated cell-death
    Shaofei Chen, Zhiyong Wang
    Frontiers in Immunology.2025;[Epub]     CrossRef
  • Mitochondrial lipid metabolism in tumor immunosurveillance and evasion
    Ana Belén Plata-Gómez, Weixin Chen, Ping-Chih Ho, Guang Sheng Ling
    Trends in Immunology.2025; 46(12): 766.     CrossRef
  • The Role of Ferroptosis on the Pathogenesis and Therapy of Hepatocellular Carcinoma
    Xue Wang, Jinhong Wang, Wentong Li, Shanming Sun
    Cell Biochemistry and Function.2025;[Epub]     CrossRef
  • Innate immunity in tumors: roles and therapeutic targets
    Songze Leng, Yuyue Ren, Yaoyao Tian, Weiwei Zhao, Yue Mou, Xingyu Chen, Hong Zhou, Wei Wang
    Frontiers in Immunology.2025;[Epub]     CrossRef
  • Ferroptosis in cancer: metabolism, mechanisms and therapeutic prospects
    Yansheng Wu, Hao Li, Kai Yue, Chao Jing, Yuansheng Duan
    Molecular Cancer.2025;[Epub]     CrossRef
  • NEFA Promotes Bovine Granulosa Cell Apoptosis via Activation of the PERK/eIF2α/ATF4/CHOP Pathway
    Jiaxing Guo, Shenghong Zhang, Yunfei Zhai, Cheng Wang, Min Liu, Lian Li
    Veterinary Sciences.2025; 12(12): 1186.     CrossRef
  • 11,918 View
  • 406 Download
  • 13 Web of Science
  • Crossref

Correspondence

Viral hepatitis

Correspondence to editorial on “Adverse impact of metabolic dysfunction on fibrosis regression following direct-acting antiviral therapy: A multicenter study for chronic hepatitis C”
Tom Ryu, Young Chang, Seung Up Kim, Jae Young Jang
Clin Mol Hepatol 2025;31(2):e203-e205.
Published online February 24, 2025
DOI: https://doi.org/10.3350/cmh.2025.0179

Citations

Citations to this article as recorded by  Crossref logo
  • Reply to correspondence on “Adverse impact of metabolic dysfunction on fibrosis regression following direct-acting antiviral therapy: A multicenter study for chronic hepatitis C”
    Chen-Hua Liu, Yu-Ping Chang
    Clinical and Molecular Hepatology.2025; 31(2): e232.     CrossRef
  • 4,820 View
  • 25 Download
  • 1 Web of Science
  • Crossref

Editorial

Viral hepatitis

Metabolic dysfunction in patients following DAA-induced viral cure for HCV infection: A non-negligible risk to liver-related health: Editorial on “Adverse impact of metabolic dysfunction on fibrosis regression following direct-acting antiviral therapy: A multicenter study for chronic hepatitis C”
Chen-Hua Liu, Yu-Ping Chang
Clin Mol Hepatol 2025;31(2):658-661.
Published online February 17, 2025
DOI: https://doi.org/10.3350/cmh.2025.0155

Citations

Citations to this article as recorded by  Crossref logo
  • Correspondence to editorial on “Adverse impact of metabolic dysfunction on fibrosis regression following direct-acting antiviral therapy: A multicenter study for chronic hepatitis C”
    Tom Ryu, Young Chang, Seung Up Kim, Jae Young Jang
    Clinical and Molecular Hepatology.2025; 31(2): e203.     CrossRef
  • Reply to correspondence on “Adverse impact of metabolic dysfunction on fibrosis regression following direct-acting antiviral therapy: A multicenter study for chronic hepatitis C”
    Chen-Hua Liu, Yu-Ping Chang
    Clinical and Molecular Hepatology.2025; 31(2): e232.     CrossRef
  • Viral oncogenesis and immune remodeling: Decoding the therapeutic potential of immune checkpoint inhibitors in virus-associated cancers
    Lihua Qi, Bai Hu, Canhui Cao, Ting Peng, Miaochun Xu, Shiyi Liu, Yashi Xu, Xiaojie Liu, Wencheng Ding, Li Li, Shitong Lin
    Biomedicine & Pharmacotherapy.2025; 191: 118515.     CrossRef
  • 6,194 View
  • 52 Download
  • 2 Web of Science
  • Crossref

Original Articles

Viral hepatitis

Adverse impact of metabolic dysfunction on fibrosis regression following direct-acting antiviral therapy: A multicenter study for chronic hepatitis C
Tom Ryu, Young Chang, Soung Won Jeong, Jeong-Ju Yoo, Sae Hwan Lee, Sang Gyune Kim, Young Seok Kim, Hong Soo Kim, Seung Up Kim, Jae Young Jang
Clin Mol Hepatol 2025;31(2):548-562.
Published online January 9, 2025
DOI: https://doi.org/10.3350/cmh.2024.0904
Background/Aims
Direct-acting antivirals (DAAs) effectively eradicate hepatitis C virus. This study investigated whether metabolic dysfunction influences the likelihood of fibrosis regression after DAA treatment in patients with chronic hepatitis C (CHC).
Methods
This multicenter, retrospective study included 8,819 patients diagnosed with CHC who were treated with DAAs and achieved a sustained virological response (SVR) between January 2014 and December 2022. Fibrosis regression was defined as a 20% reduction in noninvasive surrogates for liver fibrosis, such as liver stiffness (LS) measured by vibration-controlled transient elastography (VCTE) and the fibrosis-4 (FIB-4) score. Hypercholesterolemia (h-TC) was defined as >200 mg/dL.
Results
The median age of the study population was 59.6 years, with a predominance of male patients (n=4,713, 57.3%). Genotypes 1, 2, and others were confirmed in 3,872 (46.2%), 3,487 (41.6%), and 1,024 (12.2%) patients, respectively. Diabetes mellitus (DM) was present in 1,442 (17.2%) patients and the median LS was 7.50 kPa (interquartile range, 5.30–12.50). Multivariate analysis revealed that the presence of DM and pre-DAA h-TC were independently associated with a decreased probability of fibrosis regression by VCTE. Additionally, pre-DAA h-TC was independently associated with a decreased probability of fibrosis regression by the FIB-4.
Conclusions
Metabolic dysfunction has an unfavorable influence on fibrosis regression in patients with CHC who achieve SVR after DAA treatment.

Citations

Citations to this article as recorded by  Crossref logo
  • Editorial: Risk of Incident Type 2 Diabetes and Prediabetes in Patients With Direct Acting Antiviral‐Induced Cure of Hepatitis C Virus Infection—Authors' Reply
    Yu‐Ping Chang, Jia‐Horng Kao, Chen‐Hua Liu
    Alimentary Pharmacology & Therapeutics.2025; 61(9): 1553.     CrossRef
  • Epidemiologic Characteristics of Chronic Hepatitis B and Coinfections with Hepatitis C Virus or Human Immunodeficiency Virus in South Korea: A Nationwide Claims-Based Study Using the Korean Health Insurance Review and Assessment Service Database
    Hyunwoo Oh, Won Sohn, Na Ryung Choi, Hyo Young Lee, Yeonjae Kim, Seung Woo Nam, Jae Yoon Jeong
    Pathogens.2025; 14(7): 715.     CrossRef
  • 9,232 View
  • 153 Download
  • 6 Web of Science
  • Crossref
Plasma lipidomics and fungal peptide-based community analysis identifies distinct signatures for early mortality in acute liver failure
Neha Sharma, Sushmita Pandey, Gaurav Tripathi, Manisha Yadav, Nupur Sharma, Babu Mathew, Abhishak Gupta, Vasundhra Bindal, Sadam H. Bhat, Yash Magar, Rimsha Saif, Sanju Yadav, Amritpal Kaur, Rakhi Maiwall, Shvetank Sharma, Shiv Kumar Sarin, Jaswinder Singh Maras
Clin Mol Hepatol 2025;31(4):1233-1251.
Published online December 13, 2024
DOI: https://doi.org/10.3350/cmh.2024.0554
Background/Aims
Acute liver failure (ALF) has high mortality predominantly due to compromised immune system and increased vulnerability to bacterial and fungal infections.
Methods
Plasma lipidome and fungal peptide-based community (mycobiome) analysis were performed in discovery cohort (ALF=40, healthy=5) and validated in a validation cohort of 230 patients with ALF using high-resolution-mass-spectrometry, artificial neural network (ANN) and machine learning (ML).
Results
Untargeted lipidomics identified 2,013 lipids across 8 lipid group. 5 lipid-species—phosphatidylcholine (PC)[15:0/17:0], PC[20:1/14:1], PC[26:4/10:0], PC[32:0] and TG[4:0/10:0/23:6]—significantly differentiated ALF-NS (FC>10, P<0.05, FDR<0.01). Mycobiome alpha/beta diversity was significantly higher and showed 4 phyla and >20 species significantly dysregulated in ALF-NS linked with lipid metabolism, fatty acid elongation in ER, and others (P<0.05). Lipid and mycobiome diversity values in ALF-NS were strongly correlated (r2>0.7, P<0.05). Multi-modular correlation network showed striking associations between lipid, fungal peptide modules, and clinical parameters specific to ALF-NS (P<0.05). Cryptococcus amylolentus CBS6039 and Penicillium oxalicum 1142 directly correlated with phosphatidylcholine, triglycerides, and severity in ALF-NS (r2>0.85, P<0.05). POD-fungus and POD-lipids showed direct association with infection, necrosis, and hepatic encephalopathy (Beta>1.2, P<0.05). POD-lipid (AUC=0.969 and HR=1.99 [1.02–2.04]) superseded POD-fungus and severity indices for early-mortality prediction. Finally, significant increase in PC (15:0/17:0) level showed highest normalized importance, and ANNs and ML predicted early mortality with >95% accuracy, sensitivity, and specificity. Interestingly, fungal surveillance protein Clec7a was significantly downregulated (>2-fold), leading to a notable increase in fungal infection-mediated choline/phosphatidylcholine and associated enzymes (FC>1.5; Kennedy cycle). This contributed to phosphatidic acid-mediated hyper-inflammation in ALF-NS.
Conclusions
In ALF, the plasma lipidome and mycobiome are dysregulated. Increased circulating phosphatidylcholine could stratify ALF predisposed to early mortality or require emergency liver transplantation.

Citations

Citations to this article as recorded by  Crossref logo
  • Acute-on-chronic liver failure: pathophysiological mechanisms and clinical management
    S. K. Sarin, Ashok Choudhury, Anupam Kumar, Nadim Mahmud, G. H. Lee, Qin Ning, Soek-Siam Tan, Kessarin Thanapirom, Vinod Arora, Nobuaki Nakayama, Jun Li, Constantine J. Karvellas
    Nature Reviews Gastroenterology & Hepatology.2026;[Epub]     CrossRef
  • Plasma lipidomic and fungal signatures predict early mortality in acute liver failure
    Yu Ji Kim, Jong-Won Kim
    Clinical and Molecular Hepatology.2026; 32(1): e21.     CrossRef
  • 10,305 View
  • 283 Download
  • 2 Web of Science
  • Crossref

Steatotic liver disease

USP29 alleviates the progression of MASLD by stabilizing ACSL5 through K48 deubiquitination
Sha Hu, Zhouxiang Wang, Kun Zhu, Hongjie Shi, Fang Qin, Tuo Zhang, Song tian, Yanxiao Ji, Jianqing Zhang, Juanjuan Qin, Zhigang She, Xiaojing Zhang, Peng Zhang, Hongliang Li
Clin Mol Hepatol 2025;31(1):147-165.
Published online October 2, 2024
DOI: https://doi.org/10.3350/cmh.2024.0478
Background/Aims
Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression.
Methods
USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes.
Results
USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5.
Conclusions
USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.

Citations

Citations to this article as recorded by  Crossref logo
  • RNF90 promotes hepatic steatosis by degrading CPT1α to suppress fatty acid oxidation
    Feng-Juan Yan, Ning Zhang, Shu-Han Li, Mei-Xin Huang, Meng-Meng Wu, Yu-Jie Yan, Xin Liu, Hao Lei
    Journal of Biological Chemistry.2026; : 111231.     CrossRef
  • Metabolic-Dysfunction-Associated Steatotic Liver Disease: Molecular Mechanisms, Clinical Implications, and Emerging Therapeutic Strategies
    Jeysson E. Mejía-Guzmán, Ramón A. Belmont-Hernández, Norberto C. Chávez-Tapia, Misael Uribe, Natalia Nuño-Lámbarri
    International Journal of Molecular Sciences.2025; 26(7): 2959.     CrossRef
  • Stabilizing hepatic fatty acid oxidation: Editorial on “USP29 alleviates the progression of MASLD by stabilizing ACSL5 through K48 deubiquitination”
    Myeung Gi Choi, Na Young Lee, Ja Hyun Koo
    Clinical and Molecular Hepatology.2025; 31(2): 592.     CrossRef
  • Association Between Visceral Adiposity and the Prediction of Hepatic Steatosis and Fibrosis in Patients with Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD)
    Renata Bende, Darius Heredea, Iulia Rațiu, Ioan Sporea, Mirela Dănilă, Roxana Șirli, Alina Popescu, Felix Bende
    Journal of Clinical Medicine.2025; 14(10): 3405.     CrossRef
  • Alisol B ameliorated metabolic dysfunction-associated steatotic liver disease via regulating purine metabolism and restoring the gut microbiota disorders
    Lin Yiyou, Zhang Congcong, Ren Guilin, Qiu Jiannan, Fu Yilong, Liu Fucai, Liu Qingsheng, Yu Zhiling, Chen Lin, Dou Xiaobing
    Phytomedicine.2025; 145: 156992.     CrossRef
  • ELAVL1-mediated USP29 mRNA degradation activates TAK1 driving M1 microglial polarization and neural stem cell differentiation dysregulation in spinal cord injury
    Chunhe Sha, Feng Pan, Xiaodong Liu, Zhiqing Wang, Guohui Liu, Kai Huang
    Cell Death Discovery.2025;[Epub]     CrossRef
  • Pemafibrate Ameliorates Steatotic Liver Disease Regardless of Endothelial Dysfunction in Mice
    Tomoyo Hara, Hiroki Yamagami, Ryoko Uemoto, Akiko Sekine, Yousuke Kaneko, Kohsuke Miyataka, Taiki Hori, Mayuko Ichimura-Shimizu, Masafumi Funamoto, Takeshi Harada, Tomoyuki Yuasa, Shingen Nakamura, Itsuro Endo, Ken-ichi Matsuoka, Yutaka Kawano, Koichi Tsu
    Antioxidants.2025; 14(7): 891.     CrossRef
  • Ubiquitination and ubiquitin-like modifications in metabolic dysfunction-associated steatotic liver disease: mechanisms and implications
    Hyunjin Rho, Uijin Kim, Jaewhan Song
    BMB Reports.2025; 58(9): 371.     CrossRef
  • USP2 promotes metabolic dysfunction-associated steatotic liver disease progression via stabilization of PPARγ
    Hao Luo, Chujiao Zhu, Yingying Wang, Yidong Dai, Peng Hao, Haiyan Cai, Wenhui Bai, Zhenge Zhang, Jiale Wan, Youping Zhang, Yun Sun, Ziwei Zhang, Yunzhao Wu, Yuanhui Zhai, Wenxuan Wu, Hu Lei, Hanzhang Xu, Ming He, Yingli Wu
    Cell Death & Differentiation.2025;[Epub]     CrossRef
  • Obesity-Driven Metabolic Disorders: The Interplay of Inflammation and Mitochondrial Dysfunction
    Wooyoung Choi, Gun Ha Woo, Tae-Hwan Kwon, Jae-Han Jeon
    International Journal of Molecular Sciences.2025; 26(19): 9715.     CrossRef
  • Posttranslational modifications in Helicobacter pylori-associated gastric pathogenesis: Bridging inflammation and carcinogenesis
    Wei Li, Tong Liu, Tianhua Wu, Ting Cai, Fen Wang, Minglin Zhang
    Biochimica et Biophysica Acta (BBA) - Reviews on Cancer.2025; 1880(6): 189492.     CrossRef
  • Deubiquitinases in liver diseases: from mechanisms to targeted therapy
    Zhenge Zhang, Wanli Duan, Yixiang Wang, Peng Hao, Linlin Chen, Ziyi Hao, Ming He, Yingli Wu, Hao Luo
    Science China Life Sciences.2025;[Epub]     CrossRef
  • 9,511 View
  • 677 Download
  • 13 Web of Science
  • Crossref

Correspondence

Viral hepatitis

Letter: Cardiovascular risk of tenofovir disoproxil fumarate or tenofovir alafenamide fumarate in patients with chronic hepatitis B: More questions than an answer – author’s reply
Hyeyeon Hong, Jonggi Choi
Clin Mol Hepatol 2024;30(2):272-273.
Published online February 21, 2024
DOI: https://doi.org/10.3350/cmh.2024.0123

Citations

Citations to this article as recorded by  Crossref logo
  • Reply to correspondence on “Cardiovascular risk in chronic hepatitis B patients treated with tenofovir disoproxil fumarate or tenofovir alafenamide”
    Pin-Nan Cheng, Ming-Lung Yu
    Clinical and Molecular Hepatology.2024; 30(4): 1031.     CrossRef
  • 5,735 View
  • 90 Download
  • 1 Web of Science
  • Crossref

Original Article

Viral hepatitis

Cardiovascular risk in chronic hepatitis B patients treated with tenofovir disoproxil fumarate or tenofovir alafenamide
Hyeyeon Hong, Won-Mook Choi, Danbi Lee, Ju Hyun Shim, Kang Mo Kim, Young-Suk Lim, Han Chu Lee, Jonggi Choi
Clin Mol Hepatol 2024;30(1):49-63.
Published online November 20, 2023
DOI: https://doi.org/10.3350/cmh.2023.0328
Background/Aims
Tenofovir disoproxil fumarate (TDF) is known to have a lipid-lowering effect. This is in contrast to tenofovir alafenamide (TAF), which has a lipid-neutral effect. Therefore, concerns have been raised as to whether these differences affect long-term cardiovascular risk. Here, we aimed to evaluate the long-term risk of cardiovascular events in chronic hepatitis B (CHB) patients treated with TAF or TDF.
Methods
We retrospectively analyzed 4,124 treatment-naïve CHB patients treated with TDF (n=3,186) or TAF (n=938) between 2012 and 2022. The primary outcome was a composite endpoint of major adverse cardiovascular events (MACE), including myocardial infarction, ischemic stroke, and hospitalization for unstable angina or heart failure. Serial changes in lipid profiles between two treatments were also explored.
Results
The median age of the patients was 50.6 years, and 60.6% of the patients were male. At baseline, 486 (11.8%) and 637 (15.4%) of the patients had dyslipidemia and fatty liver, respectively. A total of 42 MACE occurred, with an annual incidence of 0.2%/100 person-years (PYs). At 1, 3, and 5 years, the cumulative risk of MACE was 0.4%, 0.8%, and 1.2% in patients treated with TDF, and 0.2%, 0.7%, and 0.7% in patients treated with TAF, respectively (p=0.538). No significant differences in the risk of MACE were observed between TDF and TAF. A multivariable analysis found that current smoker and a history of cardiovascular events were risk factors associated with an increased risk of MACE.
Conclusions
Patients treated with TAF had comparable risks of cardiovascular outcomes, defined as MACE, as patients treated with TDF.

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Review

Impact of diabetes, obesity, and dyslipidemia on the risk of hepatocellular carcinoma in patients with chronic liver diseases
Hwang Sik Shin, Baek Gyu Jun, Sang-Wook Yi
Clin Mol Hepatol 2022;28(4):773-789.
Published online August 8, 2022
DOI: https://doi.org/10.3350/cmh.2021.0383
Despite the increasing prevalence of metabolic disorders, the potential effects of metabolic factors on hepatocellular carcinoma (HCC) development in individuals with chronic liver diseases (CLDs) are not well understood. For a metabolic factor to be identified as a risk factor for HCC in patients with CLDs, such as hepatitis B virus (HBV) and hepatitis C virus (HCV) infection, there should be a strong synergistic interaction between the carcinogenic mechanisms of the metabolic factor and the CLD itself. This review aims to comprehensively summarize the published data on the relationship between metabolic factors such as diabetes mellitus (DM), obesity, and blood lipids and the risk of HCC in patients with CLDs. DM consistently increases the risk of HCC in patients with CLD. When associated with DM, the risk of HCC seems to be highest in HCV and non-alcoholic fatty liver disease (NAFLD), followed by alcoholic liver disease (ALD) and HBV. Obesity may increase the risk of HCC. Among CLDs, the evidence is relatively consistent and clear for ALD, while clear evidence is limited in other CLDs including HBV, HCV, and NAFLD. Total cholesterol, potentially low-density lipoprotein cholesterol and triglyceride, seems to have strong inverse associations with HCC in individuals with CLDs. Despite evidence from observational studies, statins had no effect in preventing HCC in randomized controlled trials. Whether statins have a preventive effect against HCC is unclear. A better understanding and management of metabolic factors may be beneficial to reduce the risk of HCC in patients with CLDs.

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Original Article

Auranofin attenuates hepatic steatosis and fibrosis in nonalcoholic fatty liver disease via NRF2 and NF- κB signaling pathways
Seung Min Lee, Dong Hee Koh, Dae Won Jun, Yoon Jin Roh, Hyeon Tae Kang, Ju Hee Oh, Hyun Sung Kim
Clin Mol Hepatol 2022;28(4):827-840.
Published online June 22, 2022
DOI: https://doi.org/10.3350/cmh.2022.0068
Background/Aims
We aim to evaluate the effects of auranofin, a known antioxidant, on hepatic steatosis, inflammation, and fibrosis, contributing to non-alcoholic steatohepatitis (NASH) development in vivo and in vitro.
Methods
Transcriptome analysis of LX-2 cells was that expression patterns of genes changed by auranofin, and their related pathways were estimated. We used the gene set enrichment analysis (GSEA) program to determine the pathway involved in overall genetic change. In vitro, LX-2 and HepG2 cells were treated with transforming growth factor (TGF)-β1 and palmitic acid (PA), respectively, and the antifibrotic and antiadipogenic effect function of auranofin was evaluated.
Results
Transcriptome analysis revealed that auranofin decreased the expression of 15 genes, including thrombospondin 1, endothelin 1 (ET-1), fibronectin 1, and LOX. The molecular functions of these genes are involved in collagen binding. GSEA of the overall gene expression pattern revealed that many genes increased in the reactive oxygen species pathway and decreased in the inflammatory response. Auranofin decreased nuclear factor kappa B (NF-κB) and IκBα in TGF-β1-induced LX-2 cells, thereby reducing ET-1 and fibrosis. Furthermore, increased pNRF2 in PA-induced HepG2 cells led to increased antioxidant marker expression and decreased lipid accumulation. In the bile duct ligation model mice, auranofin reduced the fibrosis area and increased the survival rate. Auranofin reduced liver fibrosis and lipid accumulation in NASH model mice fed on a Western diet.
Conclusions
Auranofin inhibits lipogenesis and fibrosis formation and is a proposed candidate for NASH treatment.

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Editorial

Viral hepatitis

Dyslipidemia in chronic hepatitis B patients on tenofovir alafenamide: Facts and puzzles
Hung-Yao Lin, Tai-Chung Tseng
Clin Mol Hepatol 2022;28(2):181-182.
Published online February 21, 2022
DOI: https://doi.org/10.3350/cmh.2022.0028

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  • Tenofovir Disoproxil Fumarate Versus Entecavir: Effects on Lipid Profiles and Cardiovascular Outcomes in People Living With Chronic Hepatitis B
    Log Young Kim, Jae Young Kim, Jeong‐Ju Yoo, Sang Gyune Kim, Young‐Seok Kim
    Journal of Medical Virology.2025;[Epub]     CrossRef
  • Safety of tenofovir alafenamide in the context of hyperlipidemia and cardiovascular diseases: a nationwide analysis
    Jae-Young Kim, Hyuk Kim, Jeong-Ju Yoo, Sang Gyune Kim, Young-Seok Kim
    Hepatology International.2025; 19(4): 959.     CrossRef
  • Long-Term Safety and Efficacy of Tenofovir Alafenamide in Chronic Hepatitis B: Raising the Need for Studies on Functional Cure—Editorial on “Long-Term Real-World Outcomes of Tenofovir Alafenamide in Chronic Hepatitis B”
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Letter to the Editor

Liver fibrosis, cirrhosis, and portal hypertension

Letter: cervicocerebral atherosclerosis and its hepatic and coronary risk factors in patients with liver cirrhosis
Yi-Chun Huang, Chih-Wei Chen, James Chun-Chung Wei
Clin Mol Hepatol 2022;28(2):265-266.
Published online January 4, 2022
DOI: https://doi.org/10.3350/cmh.2021.0412

Citations

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  • Reply: Letter: cervicocerebral atherosclerosis and its hepatic and coronary risk factors in patients with liver cirrhosis
    Jihyun An, Ju Hyun Shim
    Clinical and Molecular Hepatology.2022; 28(2): 267.     CrossRef
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Original Article

Viral hepatitis

Tenofovir alafenamide treatment may not worsen the lipid profile of chronic hepatitis B patients: A propensity score-matched analysis
Joonho Jeong, Jung Woo Shin, Seok Won Jung, Eun Ji Park, Neung Hwa Park
Clin Mol Hepatol 2022;28(2):254-264.
Published online December 28, 2021
DOI: https://doi.org/10.3350/cmh.2021.0314
Background/Aims
Tenofovir alafenamide (TAF) has shown less favorable effect on lipids compared to tenofovir disoproxil fumarate (TDF) in clinical trials. However, data regarding these outcomes in patients with chronic hepatitis B (CHB) are scarce. Therefore, this study aimed to evaluate the effect of TAF on the lipid in patients with CHB.
Methods
A total of 237 TAF-treated CHB patients compared with TDF, inactive CHB, and non-hepatitis B virus (HBV)-infected control groups using propensity score matching (PSM).
Results
Following PSM, each analysis was conducted on cohorts via the matching of 70:140 (TAF:TDF), 89:89 (TAF:inactive CHB), 140:560 (TAF:non-HBV infected control), and 368:1,472 (TDF:non-HBV-infected control). A significant decrease in the total cholesterol (TC) level was noted at 48 weeks in the TDF group compared to the TAF group (176.3±32.9 vs. 156.7±27.7, P<0.001) and the non-HBV-infected control group (175.0±29.5 vs. 156.2±28.3, P<0.001). However, no significant change in TC was observed in the TAF group and inactive CHB or non-HBV-infected control groups at 48 weeks. For the subgroup analyses of TAF vs. non-HBV-infected control subjects and inactive CHB patients whose detailed lipid profile information were available, no between-group differences in TC, low-density lipoprotein (LDL)-cholesterol, highdensity lipoprotein (HDL)-cholesterol, TC/HDL ratio, and LDL/HDL ratio were observed at 48 weeks.
Conclusions
TDF seems to have a lipid-lowering effect compared to the non-HBV-infected control and TAF-treated groups. However, in real practice, TAF might not worsen the lipid profiles of subjects compared to non-HBV-infected controls and patients with inactive CHB.

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Review

Steatotic liver disease

Recent advances in nonalcoholic fatty liver disease metabolomics
Hwi Young Kim
Clin Mol Hepatol 2021;27(4):553-559.
Published online June 8, 2021
DOI: https://doi.org/10.3350/cmh.2021.0127
The clinical phenotypes of nonalcoholic fatty liver disease (NAFLD) encompass from simple steatosis to nonalcoholic steatohepatitis (NASH) with varying degrees of fibrosis or cirrhosis. Liver biopsy has been the standard to diagnose NASH. However, there has been strong need for precise and accurate noninvasive tests because of invasiveness and sampling variability of biopsy. Metabolomics has drawn attention as a promising diagnostic methodology in the field of NAFLD, particularly to unravel metabolic alterations which plays relevant roles in the progression of NASH. There have been numerous metabolomics researches to find new biomarker of NASH in the last decade, fueled by the recent advances in the metabolomics methodology. This review briefly covers recent research advances on the lipidomics, amino acids and bile acid metabolomics regarding continuing attempts to discover relevant biomarkers for NASH.

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Original Articles

Viral hepatitis

The impact of pegylated interferon and ribavirin combination treatment on lipid metabolism and insulin resistance in chronic hepatitis C patients
Hee Jae Jung, Young Seok Kim, Sang Gyune Kim, Yun Nah Lee, Soung Won Jeong, Jae Young Jang, Sae Hwan Lee, Hong Soo Kim, Boo Sung Kim
Clin Mol Hepatol 2014;20(1):38-46.
Published online March 26, 2014
DOI: https://doi.org/10.3350/cmh.2014.20.1.38
Background/Aims

Lipid profile and insulin resistance (IR) are associated with hepatitis C virus (HCV) and may predict the chronic hepatitis C (CHC) treatment response. The aim of this study was to determine the association between CHC treatment response and lipid profile and IR change during treatment.

Methods

In total, 203 CHC patients were reviewed retrospectively between January 2005 and December 2011 at Soon Chun Hyang University Hospital. The lipid profile, homeostasis model for assessment (HOMA) of IR (HOMA-IR), and HOMA of β cells (HOMA-β) were evaluated before interferon plus ribavirin therapy (BTx), at the end of treatment (DTx), and 24 weeks after the end of treatment (ATx).

Results

A sustained virologic response (SVR) was achieved by 81% of all patients (49/60), 60% (n=36) of whom possessed genotype 1, with the remainder being non-genotype-1 (40%, n=24). Apart from age, which was significantly higher in the non-SVR group (SVR, 48.0±11.2 years, mean±SD; non-SVR, 56.6±9.9 years; P<0.01), there were no significant differences in the baseline characteristics between the SVR and non-SVR groups. In the SVR group, low density lipoprotein-cholesterol (LDL-C) had significantly changed at DTx and ATx compared to BTx. In addition, HOMA-IR and HOMA-β were significantly changed at DTx in the SVR group. Among those with a high baseline insulin resistance (HOMA-IR >2.5), HOMA-IR was significantly changed at DTx in the SVR group.

Conclusions

LDL-C appears to be associated with HCV treatment in SVR patients. Furthermore, eradication of HCV may improve whole-body IR and insulin hypersecretion, as well as high baseline insulin resistance (HOMA-IR >2.5).

Citations

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Lipid Peroxidation in Chronic Liver Diseases Type B
Kyung Chul Kim , Kwan Sik Lee , Kwang Hyub Han , Won Choi , Chae Yoon Chon , Sang In Lee , Young Myung Moon , Jin Kyung Kang , In Suh Park , Hye Young Kim
Korean J Hepatol 1997;3(1):40-49.
Background/Aims
.' Oxidative stress is known to play a role in the pathogenesis of a certain liver diseases such as alcoholic liver disease, metal storage disease, and ischemia/reperfusion injury. Recently oxidative stress(lipid peroxidation) has also been implicated in hepatic fibrosis, which is now regarded as a common response to chronic liver injury regardless of its nature. Development of fibrosis and cirrhosis are the major complications of chronic hepatitits B. So we aimed to detect lipid peroxidation in chronic hepatitis B and to investigate its potential role in the pathophysiology of the disease. Methods .' The subjects were histologically-proven 56 patients, including fatty liver(FL, n=8), healthy HBsAg carrier(n=6), chronic persistent hepatitis(CPH, n=8), mild chronic active hepatitis(CAH- m, n=10), severe CAH(CAH-s, n=16), and liver cirrhosis(LC, n=8). All patients were serologically HBsAg-positive except those with FL. Lipid peroxidation was detected in serum and liver specimen with TBARS(thiobarbituric acid-reacting substances) assay. Western blot and immunohistochemical stain of liver specimen were also performed, using polyclonal antibody against malondialdehyde (MDA). Results '. 1. There were no significant differences in serum TBARS levels among groups(p= 0.24). 2. The mean tissue TBARS level(nmol/g) was significantly higher in CAH-s group(175.4+ 41.5) than in other groups(FL 54.0+ 6.4, Carrier 51.1+ 15.9, CPH 63.9+ 2.9, CAH-m 68.9+ 7.9, LC 22.6+ 5.1) (p<0.05). 3. Tissue TBARS levels correlated with serum ALT levels(r=0.5934, p<0.05). 4. Western blot showed MDA bands only in CAH-s group. 5. Immunohistochemistry showed a strong MDA stain around portal and periportal area in CAH-s group, but weak or no stain in other groups. Conclusions . This study shows that lipid peroxidation can be detected in situ and commonly occurs in severe chronic hepatitis B. Oxidative stress may be related to active necroinflammatory change of the liver and contribute to the progression of the disease in chronic hepatitis B.
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Liver Pathology
Drug Induced Hepatitis Mimicking Alcoholic Hepatitis
Dae-Young Kang, M.D. and So-Young Jin, M.D.1
Korean J Hepatol 2006;12(4):574-578.
  • 3,502 View
  • 21 Download
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