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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
Animal Models and Experimental Medicine – Wiley
Published: May 18, 2023
Keywords: AMPK; apoptosis; hepatic stellate cell; liver fibrosis; perilipin 5
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