Autocrine GDF10 inhibits hepatic stellate cell activation via BMPR2/ALK3 receptor to prevent liver fibrosis

Published: 25 June 2024| Version 1 | DOI: 10.17632/3zn972d6r4.1
yinliang zhang


Liver fibrosis prevalence is increasing globally, thus burdening public health. Currently, there is no specific treatment for liver fibrosis. HSC activation is the predominant driver of liver fibrogenesis and the current focus in antifibrotic drug discovery. Following injury, the liver undergoes changes in its gene expression and secretion profile. Autocrine and paracrine signaling within the liver represent an important class of mediators responsible for activating HSCs. Nevertheless, the intrahepatic signals that modulate HSC activation are poorly understood. This study showed that GDF10 is an HSC-specific cytokine in the liver and exerts an antifibrotic effect by inhibiting HSC activation, suggesting that GDF10 is a novel target for treating liver fibrosis.



Tianjin Medical University


Liver Fibrosis