Mechanosignaling via Integrins: Pivotal Players in Liver Fibrosis Progression and Therapy
Sharip A. Kunz J.
February 2025Multidisciplinary Digital Publishing Institute (MDPI)
Cells
2025#14Issue 4
Liver fibrosis, a consequence of chronic liver injury, represents a major global health burden and is the leading cause of liver failure, morbidity, and mortality. The pathological hallmark of this condition is excessive extracellular matrix deposition, driven primarily by integrin-mediated mechanotransduction. Integrins, transmembrane heterodimeric proteins that serve as primary ECM receptors, orchestrate complex mechanosignaling networks that regulate the activation, differentiation, and proliferation of hepatic stellate cells and other ECM-secreting myofibroblasts. These mechanical signals create self-reinforcing feedback loops that perpetuate the fibrotic response. Recent advances have provided insight into the roles of specific integrin subtypes in liver fibrosis and revealed their regulation of key downstream effectors—including transforming growth factor beta, focal adhesion kinase, RhoA/Rho-associated, coiled-coil containing protein kinase, and the mechanosensitive Hippo pathway. Understanding these mechanotransduction networks has opened new therapeutic possibilities through pharmacological manipulation of integrin-dependent signaling.
extracellular matrix , hepatic stellate cell , Hippo pathway , integrin , liver fibrosis , mechanotransduction , MRTF , ROCK , TGF-beta , therapeutic compounds , YAP
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Department of Biomedical Sciences, Nazarbayev University School of Medicine, Astana, 020000, Kazakhstan
Laboratory of Bioinformatics and Systems Biology, National Laboratory Astana, Astana, 020000, Kazakhstan
Department of Biomedical Sciences
Laboratory of Bioinformatics and Systems Biology
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