Liver Injury and the Activation of the Hepatic Myofibroblasts
Joy X. Jiang,Natalie J. Török +1 more
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TLDR
This review focuses on the pathomechanism of stellate cell activation following chronic liver injury with the aim of identifying possible treatment targets for antifibrogenic agents.Abstract:
Liver fibrosis is a wound healing process, the end result of chronic liver injury elicited by different noxious stimuli. Activated hepatic stellate cells or myofibroblasts and portal myofibroblasts are considered the main producers of the extracellular matrix in the liver. On liver injury, the quiescent stellate cells transdifferentiate into myofibroblasts, a process highlighted by the loss of vitamin A stores, upregulation of interstitial type collagens, α-smooth muscle actin, matrix metalloproteinases, and proteoglycans, and the induction of cell survival pathways. Activation of hepatic stellate cells is a result of a complex interplay between the parenchymal cells, immune cells, extracellular matrix mechanics, and the extrahepatic milieu such as the gut microbiome. In this review we focus on the pathomechanism of stellate cell activation following chronic liver injury with the aim of identifying possible treatment targets for antifibrogenic agents.read more
Citations
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Endoplasmic Reticulum Stress in Metabolic Liver Diseases and Hepatic Fibrosis.
Jessica L. Maiers,Harmeet Malhi +1 more
TL;DR: Insight is provided into the complex signaling and regulation of the UPR, parallels and distinctions between different liver diseases, and how ER stress may be targeted as an antisteatotic or antifibrotic therapy to limit the progression of liver disease.
Journal ArticleDOI
Protective Effect of Astaxanthin on Liver Fibrosis through Modulation of TGF-β1 Expression and Autophagy
Miao Shen,Kan Chen,Jie Lu,Ping Cheng,Ling Xu,Weiqi Dai,Fan Wang,Lei He,Yan Zhang,Wang Chengfen,Jingjing Li,Jing Yang,Rong Zhu,Huawei Zhang,Yuanyuan Zheng,Yingqun Zhou,Chuanyong Guo +16 more
TL;DR: It was shown that 80 mg/kg astaxanthin had a significant protective effect on liver fibrosis by suppressing multiple profibrogenic factors.
Journal ArticleDOI
Endoplasmic reticulum stress is the crossroads of autophagy, inflammation, and apoptosis signaling pathways and participates in liver fibrosis.
TL;DR: The crossroads of autophagy, inflammation, and apoptosis signaling pathways and their participation in liver fibrosis are examined to examine the functional consequences of these alterations on ER stress and the possible involvement in Liver fibrosis.
Journal ArticleDOI
Endoplasmic reticulum stress-induced hepatic stellate cell apoptosis through calcium-mediated JNK/P38 MAPK and Calpain/Caspase-12 pathways
TL;DR: The findings showed that the Calpain/Caspase-12 activation induced by ER stress and the JNK/p38 MAPK phosphorylation induced by the increase of intracellular calcium concentration releasing from ER are the novel signaling pathway underlying the molecular mechanism of fibrosis recovery.
Journal ArticleDOI
NADPH Oxidases in Chronic Liver Diseases.
Joy X. Jiang,Natalie J. Török +1 more
TL;DR: The current advances in knowledge on the regulatory pathways of NOX activation, their cellular distribution, and their role in the modulation of redox signaling in liver diseases are summarized.
References
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