Hepatic stellate cells in the injured liver: Perspectives beyond hepatic fibrosis

2021 ◽  
Author(s):  
Devaraj Ezhilarasan
Keyword(s):  
Hepatic Fibrosis ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Injured Liver

scholarly journals Levistilide A reverses rat hepatic fibrosis by suppressing angiotensin II‑induced hepatic stellate cells activation

2020 ◽  
Vol 22 (3) ◽  
pp. 2191-2198
Author(s):  
Shu Li ◽  
Wei Zhao ◽  
Zhimin Zhao ◽  
Binbin Cheng ◽  
Shuang Li ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Hepatic Fibrosis ◽  
Hepatic Stellate Cells ◽  
Stellate Cells

Nicotinamide inhibits hepatic fibrosis by suppressing DNA synthesis and enhancing apoptosis of hepatic stellate cells

2011 ◽  
Vol 458 (6) ◽  
pp. 689-696 ◽  
Author(s):  
Jing Jin ◽  
Kyong Bun Lee ◽  
Soo Young Park ◽  
Ja-June Jang
Keyword(s):  
Dna Synthesis ◽  
Hepatic Fibrosis ◽  
Hepatic Stellate Cells ◽  
Stellate Cells

scholarly journals Adiponectin modulates focal adhesion disassembly in activated hepatic stellate cells: implication for reversing hepatic fibrosis

2014 ◽  
Vol 28 (12) ◽  
pp. 5172-5183 ◽  
Author(s):  
Pradeep Kumar ◽  
Tekla Smith ◽  
Khalidur Rahman ◽  
Jamie E. Mells ◽  
Natalie E. Thorn ◽  
...  
Keyword(s):  
Hepatic Fibrosis ◽  
Focal Adhesion ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Activated Hepatic Stellate Cells

Molecular basis for calcium signaling in hepatic stellate cells

2007 ◽  
Vol 292 (4) ◽  
pp. G975-G982 ◽  
Author(s):  
Emma A. Kruglov ◽  
Paulo R. A. V. Correa ◽  
Gaurav Arora ◽  
Jin Yu ◽  
Michael H. Nathanson ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
P2y Receptors ◽  
Type I ◽  
Inositol 1,4,5 Trisphosphate ◽  
Trisphosphate Receptor ◽  
Healthy Liver ◽  
Organ Fibrosis ◽  
Injured Liver

Progressive liver fibrosis (with the resultant cirrhosis) is the primary cause of chronic liver failure. Hepatic stellate cells (HSCs) are critically important mediators of liver fibrosis. In the healthy liver, HSCs are quiescent lipid-storing cells limited to the perisinusoidal endothelium. However, in the injured liver, HSCs undergo myofibroblastic transdifferentiation (activation), which is a critical step in the development of organ fibrosis. HSCs express P2Y receptors linking extracellular ATP to inositol (1,4,5)-trisphosphate-mediated cytosolic Ca2+ signals. Here, we report that HSCs express only the type I inositol (1,4,5)-trisphosphate receptor and that the receptor shifts into the nucleus and cell extensions upon activation. These cell extensions, furthermore, express sufficient machinery to enable local application of ATP to evoke highly localized Ca2+ signals that induce localized contractions. These autonomous units of subcellular signaling and response reveal a new level of subcellular organization, which, in turn, establishes a novel paradigm for the local control of fibrogenesis in the liver.

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