The cellular microenvironment and cytoskeletal actin dynamics in liver fibrogenesis  

作　　者：NOUR HIJAZI DON C.ROCKEY ZENGDUN SHI 

机构地区：[1]Medical University of South Carolina,Charleston,29425,USA

出　　处：《BIOCELL》2022年第9期2003-2007,共5页生物细胞（英文）

基　　金：This work was supported,in part,by the National Institute of Diabetes and Digestive and Kidney Disease(Grant No.P30 DK123704);the National Institute of General Medical Sciences(Grant No.P20 GM 130457).

摘　　要：Hepatic stellate cells(HSCs)are the primary effector cells in liver fibrosis.In the normal liver,HSCs serve as the primary vitamin A storage cells in the body and retain a“quiescent”phenotype.However,after liver injury,they transdifferentiate to an“activated”myofibroblast-like phenotype,which is associated with dramatic upregulation of smooth muscle specific actin and extracellular matrix proteins.The result is a fibrotic,stiff,and dysfunctional liver.Therefore,understanding the molecular mechanisms that govern HSC function is essential for the development of anti-fibrotic medications.The actin cytoskeleton has emerged as a key component of the fibrogenic response in wound healing.Recent data indicate that the cytoskeleton receives signals from the cellular microenvironment and translates them to cellular function—in particular,increased type I collagen expression.Dynamic in nature,the actin cytoskeleton continuously polymerizes and depolymerizes in response to changes in the cellular microenvironment.In this viewpoint,we discuss the recent developments underlying cytoskeletal actin dynamics in liver fibrosis,including how the cellular microenvironment affects HSC function and the molecular mechanisms that regulate the actininduced increase in collagen expression typical of activated HSCs.

关 键 词：Extracellular matrix Actin dynamics Transcriptional regulation SIGNALING 

分 类 号：R57[医药卫生—消化系统]