Published online Oct 26, 2015. doi: 10.4330/wjc.v7.i10.583
Peer-review started: June 3, 2015
First decision: July 6, 2015
Revised: August 31, 2015
Accepted: September 7, 2015
Article in press: September 16, 2015
Published online: October 26, 2015
Processing time: 153 Days and 0.3 Hours
Inflammation plays an essential role in the development of atherosclerosis. The initiation and growth of atherosclerotic plaques is accompanied by recruitment of inflammatory and precursor cells from the bloodstream and their differentiation towards pro-inflammatory phenotypes. This process is orchestrated by the production of a number of pro-inflammatory cytokines and chemokines. Human arterial intima consists of structurally distinct leaflets, with a proteoglycan-rich layer lying immediately below the endothelial lining. Recent studies reveal the important role of stellate pericyte-like cells (intimal pericytes) populating the proteoglycan-rich layer in the development of atherosclerosis. During the pathologic process, intimal pericytes may participate in the recruitment of inflammatory cells by producing signalling molecules and play a role in the antigen presentation. Intimal pericytes are also involved in lipid accumulation and the formation of foam cells. This review focuses on the role of pericyte-like cells in the development of atherosclerotic lesions.
Core tip: Intimal stellate cells, expressing smooth muscle α-actin that co-express antigen 3G5 antigen (known to be specific for pericytes), reside in the intima of human large arteries. There cells have been defined as “pericytes-like satellite cells” or “intimal pericytes”. Because of the peculiarities of the distribution of these cells and because of the current lack of our knowledge about the spectrum of the expression of other pericyte-associated markers in the arterial wall, it is reasonable to avoiding at this time to identify smooth muscle α-actin(+)/3G5 antigen(+) stellate-shaped cells as true pericytes. The review highlights the importance of intimal pericytes in atherosclerosis.