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. 2018 Jun 8;27(5):786–795. doi: 10.1177/0963689718779345

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© The Author(s) 2018

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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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.