AI Article Synopsis
- HIPK2 is a key regulator in fibrosis and shows increased expression in fibrotic liver tissues and TGF-β1-treated hepatic stellate cells (HSCs).
- Knockdown of HIPK2 leads to reduced HSC proliferation and lower levels of markers α-SMA and collagen I in response to TGF-β1.
- The study suggests that HIPK2 may regulate HSC activation by inhibiting the TGF-β1/Smad3 signaling pathway, indicating its potential as a target for liver fibrosis treatment.
Article Abstract
Homeodomain-interacting protein kinase 2 (HIPK2), a member of HIPKs family, is considered as a key regulator in fibrosis. However, the roles of HIPK2 in hepatic stellate cells (HSCs) activation and liver fibrosis are still unclear. Therefore, in this study, we investigated the roles of HIPK2 in HSCs activation and liver fibrosis. Our results showed that HIPK2 expression was significantly up-regulated in liver fibrotic tissues and TGF-β1-treated HSCs. Knockdown of HIPK2 significantly inhibited TGF-β1-induced HSCs proliferation, as well as decreased the expression levels of α-SMA and collagen I. Furthermore, knockdown of HIPK2 attenuated the phosphorylation of Smad3 in the presence of TGF-β1. In conclusion, these results demonstrated that HIPK2 may function as a novel regulator to modulate HSC activation, potentially by inhibiting the TGF-β1/Smad3 signaling pathway. The results provide supporting evidence that HIPK2 may be a potential target for the treatment of liver fibrosis.
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| http://dx.doi.org/10.1016/j.biopha.2016.11.066 | DOI Listing |
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