The Effect of Retinoids in Vascular Smooth Muscle Cells: From Phenotyping Switching to Proliferation and Migration

Int J Mol Sci. 2024 Sep 25;25(19):10303. doi: 10.3390/ijms251910303.

Abstract

Atherosclerosis, a term derived from the Greek "athero" (atheroma) and "sclerosis" (hardening), is a long-standing process that leads to the formation of atheromatous plaques in the arterial wall, contributing to the development of atherosclerotic cardiovascular disease. The proliferation and migration of vascular smooth muscle cells (VSMCs) and the switching of their phenotype play a crucial role in the whole process. Retinoic acid (RA), a natural derivative of vitamin A, has been used in the treatment of various inflammatory diseases and cell proliferation disorders. Numerous studies have demonstrated that RA has an important inhibitory effect on the proliferation, migration, and dedifferentiation of vascular smooth muscle cells, leading to a significant reduction in atherosclerotic lesions. In this review article, we explore the effects of RA on the pathogenesis of atherosclerosis, focusing on its regulatory action in VSMCs and its role in the phenotypic switching, proliferation, and migration of VSMCs. Despite the potential impact that RA may have on the process of atherosclerosis, further studies are required to examine its safety and efficacy in clinical practice.

Keywords: atherosclerosis; retinoic acid; vascular smooth muscle cells.

Publication types

  • Review

MeSH terms

  • Animals
  • Atherosclerosis* / drug therapy
  • Atherosclerosis* / metabolism
  • Atherosclerosis* / pathology
  • Cell Movement* / drug effects
  • Cell Proliferation* / drug effects
  • Humans
  • Muscle, Smooth, Vascular* / cytology
  • Muscle, Smooth, Vascular* / drug effects
  • Muscle, Smooth, Vascular* / metabolism
  • Myocytes, Smooth Muscle* / drug effects
  • Myocytes, Smooth Muscle* / metabolism
  • Phenotype*
  • Retinoids / pharmacology
  • Tretinoin / pharmacology

Substances

  • Retinoids
  • Tretinoin

Grants and funding

This research received no external funding.