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. 2021 Apr 1;12(2):552–569. doi: 10.14336/AD.2020.0811

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copyright: © 2021 Yan et al.

this is an open access article distributed under the terms of the creative commons attribution license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Figure 4. — Cellular senescence affects cardiac regeneration and repair. The proliferation and paracrine of senescent CMs CPCs ECs VSMCs MSCs EPCs were weaken. The decrease of CMs and CPCs attenuate myogenesis after MI. The myocardial cells in the infarct area are replaced by fibroblasts, and cardiac scars are formed. The abilities of senescent MSCs and EPCs to mobilize, migrate, differentiate, and home to the ischemic area of the heart decrease, resulting in the reduction of ECs and VSCs, which inhibit angiogenesis and cardiac repair. The senescent cells hinder angiogenesis and myogenesis after MI, leading to ventricular remodeling and heart function deteriorating, finally causing heart failure.