The migration and excessive proliferation of vascular smooth muscle cells are the common cause of many serious cardiovascular diseases. SRSF1 (serine/arginine-rich splicing factor 1) is the member of the highly conserved serine/arginine-rich protein family that functions in key aspects of mRNA metabolism. Chunmei Cao’s Team found out that the expression of SRSF1 is upregulated in the blood vessels of patients with intimal thickening, suggesting that SRSF1 is related to cardiovascular hyperplastic disorders. The further study discovered that SRSF1 regulates the expression of D133p53 through transcriptional regulation, thereby promoting the migration and proliferation of smooth muscle cells and the formation of injury-induced neointima. It reveals the regulation and mechanism of the SRSF1-D133p53-KLF5 signaling axis for the proliferation of smooth muscle cells (see Figure 1), and illustrates the important role of SRSF1 in the neointima formation through transcriptional regulation rather than splicing regulation. It can be concluded that the suppression of SRSF1 may be a new method for preventing and treating proliferative diseases.
Figure 1. Stimulating signal promotes angiogenesis by enhancing the expression of SRSF1.