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"Xiaojiaoyang Li"

Review

Acute liver injury and Acute liver failure

Current status and perspective on molecular targets and therapeutic intervention strategy in hepatic ischemia-reperfusion injury
Jia Liu, Ranyi Luo, Yinhao Zhang, Xiaojiaoyang Li
Clin Mol Hepatol 2024;30(4):585-619.
Published online July 1, 2024
DOI: https://doi.org/10.3350/cmh.2024.0222
Hepatic ischemia‒reperfusion injury (HIRI) is a common and inevitable complication of hepatic trauma, liver resection, or liver transplantation. It contributes to postoperative organ failure or tissue rejection, eventually affecting patient prognosis and overall survival. The pathological mechanism of HIRI is highly complex and has not yet been fully elucidated. The proposed underlying mechanisms include mitochondrial damage, oxidative stress imbalance, abnormal cell death, immune cell hyperactivation, intracellular inflammatory disorders and other complex events. In addition to serious clinical limitations, available antagonistic drugs and specific treatment regimens are still lacking. Therefore, there is an urgent need to not only clarify the exact etiology of HIRI but also reveal the possible reactions and bottlenecks of existing drugs, helping to reduce morbidity and shorten hospitalizations. We analyzed the possible underlying mechanism of HIRI, discussed various outcomes among different animal models and explored neglected potential therapeutic strategies for HIRI treatment. By thoroughly reviewing and analyzing the literature on HIRI, we gained a comprehensive understanding of the current research status in related fields and identified valuable references for future clinical and scientific investigations.

Citations

Citations to this article as recorded by  Crossref logo
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    Ling Shuai, Xiaojun Wang, Xudong Wen, Cong Peng, Tian Dong, Jiejuan Lai, Ling Yao, Shijun Fan, Changchun Zhao, Leida Zhang, Yujun Zhang, Xiang Xiong
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  • Feedback Loops Shape Oxidative and Immune Interactions in Hepatic Ischemia–Reperfusion Injury
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    Xinye Huang, Xiangli Zhao, Xiaosheng Tan, Yeting Zhang, Zhengyi Shi, Gang Chen, Changxing Qi, Yonghui Zhang
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  • Novel Perspectives in Hepatic Ischemia-Reperfusion Injury: The cGAS-STING Pathway
    Runsheng Chen, Tingfeng Yang, Zhonghao Jiang, Yang Long, Baolin Qian, Wenguang Fu
    Journal of Inflammation Research.2025; Volume 18: 16427.     CrossRef
  • Protective effects of treprostinil and ischemic preconditioning on hepatic ischemia-reperfusion injury and biomarkers in experimental studies in rats
    Christina Mouratidou, Efstathios T Pavlidis, Georgios Katsanos, Serafeim-Chrysovalantis Kotoulas, Maria Papaioannou, Georgios Tsoulfas, Emmanouela Apostolopoulou, Georgia D Brellou, Ioannis N Galanis, Theodoros E Pavlidis
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Correspondence

Liver fibrosis, cirrhosis, and portal hypertension

  • 6,014 View
  • 63 Download
Review

Liver fibrosis, cirrhosis, and portal hypertension

Liver sinusoidal endothelial cell: An important yet often overlooked player in the liver fibrosis
Jiaorong Qu, Le Wang, Yufei Li, Xiaojiaoyang Li
Clin Mol Hepatol 2024;30(3):303-325.
Published online February 28, 2024
DOI: https://doi.org/10.3350/cmh.2024.0022
Liver sinusoidal endothelial cells (LSECs) are liver-specific endothelial cells with the highest permeability than other mammalian endothelial cells, characterized by the presence of fenestrae on their surface, the absence of diaphragms and the lack of basement membrane. Located at the interface between blood and other liver cell types, LSECs mediate the exchange of substances between the blood and the Disse space, playing a crucial role in maintaining substance circulation and homeostasis of multicellular communication. As the initial responders to chronic liver injury, the abnormal LSEC activation not only changes their own physicochemical properties but also interrupts their communication with hepatic stellate cells and hepatocytes, which collectively aggravates the process of liver fibrosis. In this review, we have comprehensively updated the various pathways by which LSECs were involved in the initiation and aggravation of liver fibrosis, including but not limited to cellular phenotypic change, the induction of capillarization, decreased permeability and regulation of intercellular communications. Additionally, the intervention effects and latest regulatory mechanisms of anti-fibrotic drugs involved in each aspect have been summarized and discussed systematically. As we studied deeper into unraveling the intricate role of LSECs in the pathophysiology of liver fibrosis, we unveil a promising horizon that pave the way for enhanced patient outcomes.

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