Apelin/APJ system: A critical regulator of vascular smooth muscle cell

J Cell Physiol. 2018 Jul;233(7):5180-5188. doi: 10.1002/jcp.26339. Epub 2018 Jan 23.

Abstract

APJ, an orphan G protein-coupled receptor, is first identified through homology cloning in 1993. Apelin is endogenous ligand of APJ extracted from bovine stomach tissue in 1998. Apelin/APJ system is widely expressed in many kinds of cells such as endothelial cells, cardiomyocytes, especially vascular smooth muscle cell. Vascular smooth muscle cell (VSMC), an integral part of the vascular wall, takes part in many normal physiological processes. Our experiment firstly finds that apelin/APJ system enhances VSMC proliferation by ERK1/2-cyclin D1 signal pathway. Accumulating studies also show that apelin/APJ system plays a pivotal role in mediating the function of VSMC. In this paper, we review the exact role of apelin/APJ system in VSMC, including induction of proliferation and migration, enhance of contraction and relaxation, inhibition of calcification. Furthermore, we discuss the role of apelin/APJ system in vascular diseases, such as atherosclerosis, hypertension, and chronic kidney disease (CKD) from the point of VSMC. Above all, apelin/APJ system is a promising target for managing vascular disease.

Keywords: VSMCs; apelin/APJ system; atherosclerosis; chronic kidney disease; hypertension.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Apelin / genetics*
  • Apelin / metabolism
  • Apelin Receptors / genetics*
  • Apelin Receptors / metabolism
  • Atherosclerosis / genetics
  • Atherosclerosis / metabolism
  • Cell Movement / genetics
  • Cell Proliferation / genetics
  • Humans
  • Hypertension / genetics
  • Hypertension / metabolism
  • MAP Kinase Signaling System
  • Muscle, Smooth, Vascular / metabolism*
  • Muscle, Smooth, Vascular / physiopathology
  • Myocytes, Cardiac / metabolism
  • Myocytes, Cardiac / pathology
  • Myocytes, Smooth Muscle / metabolism*
  • Myocytes, Smooth Muscle / pathology
  • Renal Insufficiency, Chronic / genetics
  • Renal Insufficiency, Chronic / metabolism

Substances

  • APLNR protein, human
  • Apelin
  • Apelin Receptors