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. 2023 May 11;21:109. doi: 10.1186/s12964-023-01105-4

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© The Author(s) 2023

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Crosstalk between macrophages and cardiomyocytes (CMs). A Dead CMs induce shedding of the MERTK receptor. B Macrophages phagocytose exophers to maintain homeostasis. C Macrophages secrete OSM to promote CM proliferation through gp130/Src/Yap-Notch and Yap-ctgf/Areg pathways. D The dsDNA from CMs that have undergone cell death stimulates the cGAS-STING-IRF3 pathway to induce the apoptosis of healthy CMs. E Macrophages interact with CMs via focal adhesion complex markers (such as β-integrin) and activate TRPV4 to promote the expression of M-CSF by sensing left ventricular pressure. F CD47 expression on CMs impairs the efferocytosis by macrophages