Stellate cell contraction: role, regulation, and potential therapeutic target.
The contraction of hepatic stellate cells has been proposed to mediate fibrosis by regulating sinusoidal blood flow and extracellular matrix remodeling. Abundant data from diverse, yet complementary, experimental methods support a robust model for the regulation of contractile force generation by stellate cells. In this model, soluble factors associated with liver injury, including endothelin 1 and nitric oxide, are transduced primarily through Rho signaling pathways that promote the myosin II-powered generation of contractile force by stellate cells. The enhanced knowledge of the role and differential regulation of stellate cell contraction may facilitate the discovery of new and targeted strategies for the prevention and treatment of hepatic fibrosis.
Soon
Russell K
RK
Department of Medicine and Liver Center, University of California, San Francisco, CA 94110, USA.
Yee
Hal F
HF
D000818:Animals; D003285:Contractile Proteins / Q000378:metabolism; D019332:Endothelin-1 / Q000378:metabolism*; D005109:Extracellular Matrix / Q000378:metabolism; D055166:Hepatic Stellate Cells / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000378:metabolism; D008103:Liver Cirrhosis / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy*; D024462:Myosin Type II / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism*; D011168:Portal System / Q000378:metabolism; D015398:Signal Transduction; D054460:rho-Associated Kinases / Q000378:metabolism
D003285:Contractile Proteins; D019332:Endothelin-1; D047908:Intracellular Signaling Peptides and Proteins; D009569:Nitric Oxide; D054460:rho-Associated Kinases; D024462:Myosin Type II