Smooth muscle cells (SMCs) can be easily found in blood vessels and most hollow organs, being the major contractile component. The differentiation of SMCs is characterised by the presence of specific proteins. A switch of phenotype, from contractile to synthetic, of vascular SMCs occurs in response to vascular injuries, characterised by increased migration and proliferation as well as reduced expression of contractile proteins. In simple words, VSMCs becomes less contractile but more proliferative to facilitate injury recovery. A research team generated novel insight into the underlying molecular mechanism for the regulation of SMC phenotypic switch through the discovery of the abundance of SMC-specific RNA - CARMN in healthy SMCs. It is not surprising that CARMN expression was found reduced markedly in diseased vascular wall of both humans and mice. Deletion of CARMN in mice led to exacerbation of injury-induced neointima formation, while restoring its expression was protective against the formation. The findings have suggested increasing or maintaining CARMN expression as a potentially promising therapeutic approach to treat or prevent proliferative vascular disease, such as atherosclerosis and angioplasty-induced restenosis.

References

1. Dong K, et al. Circulation. 2021;144:1856-1875