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Perilipin 5 regulates hepatic stellate cell activation and high‐fat diet‐induced non‐alcoholic fatty liver disease

Perilipin 5 regulates hepatic stellate cell activation and high‐fat diet‐induced non‐alcoholic... INTRODUCTIONNAFLD is a chronic liver disease with a range spectrum from simple fatty liver to advanced non‐alcoholic steatohepatitis (NASH).1 About a third of patients develop hepatic fibrogenesis, even cirrhosis and hepatocellular carcinoma,2 but underlying mechanisms of pathogenesis generally remain elusive.Hepatic stellate cells (HSCs) locate between hepatocytes and sinusoidal endothelial cells and are known as the main effectors of hepatic fibrogenesis.3 In a healthy liver, HSCs stay at a quiescent state with a large number of lipid droplets (LDs) rich in retinol.4 During chronic liver damage, HSCs transdifferentiate into myofibroblast‐like cells with concomitant loss of their LDs, de novo synthesis of α‐smooth muscle actin (α‐SMA) and α1 type I collagen, leading to an imbalanced formation and degradation of extracellular matrix (ECM).4 This process is known as HSC activation, presenting a high proliferation rate and initiating liver fibrosis.4 Although advances in the understanding of genes promoting HSC activation are impressive, there are no effective therapeutic interventions available for hepatic fibrogenesis.5 As a consequence, inhibition or reversion of HSC activation or induction of apoptosis or necrosis of activated HSCs, could help in further understanding of hepatic fibrosis and suggest novel therapeutic strategies.Perilipin 5 (PLIN5), also called oxidative tissue‐enriched PAT protein (OXPAT) and lipid http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Animal Models and Experimental Medicine Wiley

Perilipin 5 regulates hepatic stellate cell activation and high‐fat diet‐induced non‐alcoholic fatty liver disease

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References (49)

Publisher
Wiley
Copyright
© 2023 The Chinese Association for Laboratory Animal Sciences.
eISSN
2576-2095
DOI
10.1002/ame2.12327
Publisher site
See Article on Publisher Site

Abstract

INTRODUCTIONNAFLD is a chronic liver disease with a range spectrum from simple fatty liver to advanced non‐alcoholic steatohepatitis (NASH).1 About a third of patients develop hepatic fibrogenesis, even cirrhosis and hepatocellular carcinoma,2 but underlying mechanisms of pathogenesis generally remain elusive.Hepatic stellate cells (HSCs) locate between hepatocytes and sinusoidal endothelial cells and are known as the main effectors of hepatic fibrogenesis.3 In a healthy liver, HSCs stay at a quiescent state with a large number of lipid droplets (LDs) rich in retinol.4 During chronic liver damage, HSCs transdifferentiate into myofibroblast‐like cells with concomitant loss of their LDs, de novo synthesis of α‐smooth muscle actin (α‐SMA) and α1 type I collagen, leading to an imbalanced formation and degradation of extracellular matrix (ECM).4 This process is known as HSC activation, presenting a high proliferation rate and initiating liver fibrosis.4 Although advances in the understanding of genes promoting HSC activation are impressive, there are no effective therapeutic interventions available for hepatic fibrogenesis.5 As a consequence, inhibition or reversion of HSC activation or induction of apoptosis or necrosis of activated HSCs, could help in further understanding of hepatic fibrosis and suggest novel therapeutic strategies.Perilipin 5 (PLIN5), also called oxidative tissue‐enriched PAT protein (OXPAT) and lipid

Journal

Animal Models and Experimental MedicineWiley

Published: May 18, 2023

Keywords: AMPK; apoptosis; hepatic stellate cell; liver fibrosis; perilipin 5

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