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Review
. 2018 May;27(5):786-795.
doi: 10.1177/0963689718779345. Epub 2018 Jun 8.

Endothelial progenitor cells in age-related vascular remodeling

Jin-Xiu Yang  1   2 , Yan-Yun Pan  1 , Xing-Xiang Wang  2 , Yuan-Gang Qiu  1 , Wei Mao  1
Affiliations
Review

Endothelial progenitor cells in age-related vascular remodeling

Jin-Xiu Yang et al. Cell Transplant. 2018 May.

Abstract

Accumulating evidence has demonstrated that endothelial progenitor cells (EPCs) could facilitate the reendothelialization of injured arteries by replacing the dysfunctional endothelial cells, thereby suppressing the formation of neointima. Meanwhile, other findings suggest that EPCs may be involved in the pathogenesis of age-related vascular remodeling. This review is presented to summarize the characteristics of EPCs and age-related vascular remodeling. In addition, the role of EPCs in age-related vascular remodeling and possible solutions for improving the therapeutic effects of EPCs in the treatment of age-related diseases are discussed.

Keywords: Endothelial progenitor cell; age; vascular remodeling.

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Conflict of interest statement

Declaration of Conflicting Interests: The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Figures

Figure 1.
Figure 1.
Involvement of EPCs in age-related vascular remodeling. (a) In the early stage of primary and secondary atherosclerosis after injury, characterized by endothelial dysfunction, endothelial progenitor cells (EPCs, mainly as late-outgrowth EPCs) can be mobilized to the injured area, penetrate the site of vessel injury, and differentiate into mature endothelial cells (ECs), replacing the dysfunctional endothelium and avoiding further atherosclerosis development. EPCs (mainly as early-outgrowth EPCs) could also repair injured ECs by secreting growth factors. (b) In advanced atherosclerosis, characterized by redundant sub-endothelial accumulation of lipids and immune cells, neointimal hyperplasia, excessive proliferation of smooth muscle cells (SMCs), matrix deposition, and foam cell formation, a widespread EPC mobilization concomitant with that of monocytes in response to inflammatory factors may, rather, promote plaque instability/vascularization.
See this image and copyright information in PMC

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