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"Non-alcoholic steatohepatitis"

Editorial

Steatotic liver disease

Non-invasive biomarkers for liver inflammation in non-alcoholic fatty liver disease: present and future
Kee-Huat Chuah, Wah-Kheong Chan
Clin Mol Hepatol 2023;29(2):401-403.
Published online February 28, 2023
DOI: https://doi.org/10.3350/cmh.2023.0062

Citations

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  • Aerobic Exercise Training Leads to MASH Resolution as Defined by the MASH Resolution Index
    Theja Channapragada, Sarah Batra, Breianna L. Hummer, Vernon M. Chinchilli, Daniel Huang, Rohit Loomba, Ian R. Schreibman, Jonathan G. Stine
    Digestive Diseases and Sciences.2025;[Epub]     CrossRef
  • Development of a machine learning-based model to predict hepatic inflammation in chronic hepatitis B patients with concurrent hepatic steatosis: a cohort study
    Fajuan Rui, Yee Hui Yeo, Liang Xu, Qi Zheng, Xiaoming Xu, Wenjing Ni, Youwen Tan, Qing-Lei Zeng, Zebao He, Xiaorong Tian, Qi Xue, Yuanwang Qiu, Chuanwu Zhu, Weimao Ding, Jian Wang, Rui Huang, Yayun Xu, Yunliang Chen, Junqing Fan, Zhiwen Fan, Xiaolong Qi,
    eClinicalMedicine.2024; 68: 102419.     CrossRef
  • Functional effects and mechanisms of Phyllanthus emblica fruit and gallic acid on metabolic diseases: Experimental evidence and clinical perspectives
    Xiaoling Gou, Yin Ding, Yamei Wu, Yiwen Tao, Yaqian Wang, Yue Wang, Jingye Liu, Mi Ma, Xianhua Zhou, Tsedien Nhamdriel, Gang Fan
    Food Bioscience.2024; 59: 104039.     CrossRef
  • Machine learning based identification potential feature genes for prediction of drug efficacy in nonalcoholic steatohepatitis animal model
    Marwa Matboli, Ibrahim Abdelbaky, Abdelrahman Khaled, Radwa Khaled, Shaimaa Hamady, Laila M. Farid, Mariam B. Abouelkhair, Noha E. El-Attar, Mohamed Farag Fathallah, Manal S. Abd EL Hamid, Gena M. Elmakromy, Marwa Ali
    Lipids in Health and Disease.2024;[Epub]     CrossRef
  • 8,361 View
  • 79 Download
  • 4 Web of Science
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Special topic: Alcoholic liver diseases
The 14th International Symposium on Alcoholic Liver and Pancreatic Diseases and Cirrhosis (ISALPDC)

Alcohol-related liver disease

Endoplasmic reticulum stress and autophagy dysregulation in alcoholic and non-alcoholic liver diseases
Yun Seok Kim, Sang Geon Kim
Clin Mol Hepatol 2020;26(4):715-727.
Published online September 22, 2020
DOI: https://doi.org/10.3350/cmh.2020.0173
Alcoholic and non-alcoholic liver diseases begin from an imbalance in lipid metabolism in hepatocytes as the earliest response. Both liver diseases share common disease features and stages (i.e., steatosis, hepatitis, cirrhosis, and hepatocellular carcinoma). However, the two diseases have differential pathogenesis and clinical symptoms. Studies have elucidated the molecular basis underlying similarities and differences in the pathogenesis of the diseases; the factors contributing to the progression of liver diseases include depletion of sulfhydryl pools, enhanced levels of reactive oxygen and nitrogen intermediates, increased sensitivity of hepatocytes to toxic cytokines, mitochondrial dysfunction, and insulin resistance. Endoplasmic reticulum (ER) stress, which is caused by the accumulation of misfolded proteins and calcium depletion, contributes to the pathogenesis, often causing catastrophic cell death. Several studies have demonstrated a mechanism by which ER stress triggers liver disease progression. Autophagy is an evolutionarily conserved process that regulates organelle turnover and cellular energy balance through decomposing damaged organelles including mitochondria, misfolded proteins, and lipid droplets. Autophagy dysregulation also exacerbates liver diseases. Thus, autophagy-related molecules can be potential therapeutic targets for liver diseases. Since ER stress and autophagy are closely linked to each other, an understanding of the molecules, gene clusters, and networks engaged in these processes would be of help to find new remedies for alcoholic and non-alcoholic liver diseases. In this review, we summarize the recent findings and perspectives in the context of the molecular pathogenesis of the liver diseases.

Citations

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  • 300 Download
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Editorial

Hepatic neoplasm

Citations

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  • The emerging age-pattern changes of patients with hepatocellular carcinoma in Korea
    Yuri Cho, Bo Hyun Kim, Joong-Won Park
    Clinical and Molecular Hepatology.2023; 29(1): 99.     CrossRef
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Review

Steatotic liver disease

NASH Therapy: omega 3 supplementation, vitamin E, insulin sensitizers and statin drugs
Stephen Caldwell
Clin Mol Hepatol 2017;23(2):103-108.
Published online May 10, 2017
DOI: https://doi.org/10.3350/cmh.2017.0103
Non-alcoholic steatohepatitis (NASH) is the more aggressive form of non-alcoholic fatty liver disease (NAFLD). NASH can progress to hepatic fibrosis, cirrhosis, portal hypertension and primary liver cancer. Therapy is evolving with a substantial number of trials of promising new agents now in progress. In this article however, we will examine data for several older forms of therapy which have been fairly extensively studied over the years: Polyunsaturated Fatty Acid (PUFA) supplements, vitamin E, insulin sensitizing agents with a focus on pioglitazone and statin agents. Early interest in PUFA derived from their potential benefit in cardio-metabolic disease and the close association of NAFLD/NASH with Metabolic Syndrome. Results have been variable although most studies show reduction of liver fat without other major effects and their effects are influenced by concomitant weight loss and underlying genetic factors. Vitamin E has had some efficacy in pediatric NASH but questionable efficacy in even mild NASH among adults. Pioglitazone has shown significant histological benefit in a number of trials but concern over side-effects (especially weight gain) have dampened enthusiasm. A newer insulin sensitizer, liraglutide, has also shown promise in a small randomized, controlled trial. Very limited data exists regarding the histological effects of the statins in NASH and these agents appear to be fairly neutral with neither clear cut benefit nor detriment. Their use is best guided by cardiovascular risks rather than liver histology.

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