Abstract
ObjectiveLiver fibrosis is a chronic liver disease caused by a variety of pathophysiological. However, there are no effective treatments to combat it. HSCs are a major source of fibrotic cells and exploring the mechanisms of HSC activation may provide new strategies for the treatment of liver fibrosis.ObjectivesTo explore the role and underlying mechanism of SLIT3 in HSCs fibrosis.ResultsGSE163211 dataset analysis identified aberrant expression of SLIT3 in NASH F1-F4 tissues and SLIT3 expression level was positively correlated with fibrosis-related proteins. In vitro experiments showed that TGF-β induced upregulation of SLIT3 in LX-2 cells. Knockdown of SLIT3 significantly inhibited TGF-β-induced α-SMA, COL1A2, and COL1A1 expression, inhibited excessive cell proliferation and migration, and suppressed YAP activity.ConclusionCollectively, our findings suggest that SLIT3 deficiency alleviates TGF-β-induced HSCs activation by inhibiting YAP activity.
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