No abstract

No abstract

As an outcome of chronic liver disease, liver fibrosis involves the activation of hepatic stellate cells (HSCs) caused by a variety of chronic liver injuries. It is important to explore approaches to inhibit the activation and proliferation of HSCs for the treatment of liver fibrosis. PLK1 is overexpressed in many human tumour cells and has become a popular drug target in tumour therapy. Therefore, further study of the function of PLK1 in the cell cycle is valid. In the present study, we found that PLK1 expression was elevated in primary HSCs isolated from CCl 4 ‐induced liver fibrosis mice and LX‐2 cells stimulated with TGF‐β1. Knockdown of PLK1 inhibited α‐SMA and Col1α1 expression and reduced the activation of HSCs in CCl 4 ‐induced liver fibrosis mice and LX‐2 cells stimulated with TGF‐β1. We further showed that inhibiting the expression of PLK1 reduced the proliferation of HSCs and promoted HSCs apoptosis in vivo and in vitro. Furthermore, we found that the Wnt/β‐catenin signalling pathway may be essential for PLK1‐mediated HSCs activation. Together, blocking PLK1 effectively suppressed liver fibrosis by inhibiting HSC activation, which may provide a new treatment strategy for liver fibrosis.

Proline-serine-threonine-phosphatase-interacting protein 2 (PSTPIP2) belongs to the Fes/CIP4 homology-Bin/Amphiphysin/Rvs (F-BAR) domain family. It exhibits lipid-binding, membrane deformation, and F-actin binding activity, suggesting broader roles at the membrane–cytoskeleton interface. PSTPIP2 is known to participate in macrophage activation, neutrophil migration, cytokine production, and osteoclast differentiation. In recent years, it has been observed to play important roles in innate immune diseases and autoinflammatory diseases (AIDs). Current research indicates that the protein tyrosine phosphatase PTP-PEST, Src homology domain-containing inositol 5’-phosphatase 1 (SHIP1), and C‐terminal Src kinase (CSK) can bind to PSTPIP2 and inhibit the development of AIDs. However, the mechanisms underlying the function of PSTPIP2 have not been fully elucidated. This article reviews the research progress and mechanisms of PSTPIP2 in AIDs. PSTPIP2 also provides a new therapeutic target for the treatment of AIDs.