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. 2021 May 7;8:679797. doi: 10.3389/fmolb.2021.679797

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Copyright © 2021 Lin, Ji, Li and Guo.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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M1/M2 macrophages and their roles in plaque calcification. Calcification occurs in both the intimal and medial layers of the artery. In the plaque microenvironment, multiple factors, such as inflammation, endoplasmic reticulum (ER) stress, osteoblastic differentiation, hyperlipidemia, and oxidative stress, drive the progression of calcification. M1 macrophages mainly contribute to microcalcification by the following ways: (1) M1 macrophages and other cells death (such as induced by ER stress) and the subsequent mineralization; (2) the pro-inflammatory cytokines and Oncostain M (OSM) secreted by M1 macrophages induce osteogenic trans-differentiation of vascular smooth muscle cells (VSMCs); and (3) ER stress promotes osteoblastic differentiation of VSMCs. M2 macrophages can induce macrocalcification by the following ways: (1) they counteract inflammation by producing anti-inflammatory cytokines such as IL-10; (2) they promote the production of extracellular matrix; and (3) they enhance osteoblastic differentiation of VSMCs.