Deleterious Anti-Inflammatory Macrophage Recruitment in Early Post-Infarction Phase

IF 8.4 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

JACC: Basic to Translational Science Pub Date : 2024-05-01 DOI:10.1016/j.jacbts.2024.01.019

Alexandre Paccalet PhD , Sally Badawi PhD , Bruno Pillot PhD , Lionel Augeul MRes , Laura Mechtouff MD, PhD , Zeina Harhous PhD , Yves Gouriou AP, PhD , Mélanie Paillard PhD , Marine Breuilly PhD , Camille Amaz MsRes , Yvonne Varillon MsRes , Simon Leboube MD , Camille Brun MsRes , Cyril Prieur MD, PhD , Gilles Rioufol MD, PhD , Nathan Mewton MD, PhD , Michel Ovize MD, PhD , Gabriel Bidaux PhD , Thomas Bochaton MD, PhD , Claire Crola Da Silva PhD

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Abstract

Using a translational approach with an ST-segment myocardial infarction (STEMI) cohort and mouse model of myocardial infarction, we highlighted the role of the secreted IL-6 and MCP-1 cytokines and the STAT3 pathway in heart macrophage recruitment and activation. Cardiac myocytes secrete IL-6 and MCP-1 in response to hypoxic stress, leading to a recruitment and/or polarization of anti-inflammatory macrophages via the STAT3 pathway. In our preclinical model of myocardial infarction, neutralization of IL-6 and MCP-1 or STAT3 pathway reduced infarct size. Together, our data demonstrate that anti-inflammatory macrophages can be deleterious in the acute phase of STEMI.

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脑梗塞后早期有害的抗炎巨噬细胞招募

我们利用ST段心肌梗死（STEMI）队列和心肌梗死小鼠模型的转化方法，强调了分泌的IL-6和MCP-1细胞因子以及STAT3通路在心脏巨噬细胞招募和活化中的作用。心肌细胞在缺氧应激时分泌 IL-6 和 MCP-1，通过 STAT3 通路导致抗炎巨噬细胞的招募和/或极化。在我们的心肌梗死临床前模型中，中和 IL-6 和 MCP-1 或 STAT3 通路可缩小梗死面积。总之，我们的数据证明，在 STEMI 急性期，抗炎巨噬细胞可能是有害的。

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来源期刊

JACC: Basic to Translational Science CARDIAC & CARDIOVASCULAR SYSTEMS-

CiteScore

14.20

自引率

1.00%

发文量

161

审稿时长

16 weeks

期刊介绍： JACC: Basic to Translational Science is an open access journal that is part of the renowned Journal of the American College of Cardiology (JACC). It focuses on advancing the field of Translational Cardiovascular Medicine and aims to accelerate the translation of new scientific discoveries into therapies that improve outcomes for patients with or at risk for Cardiovascular Disease. The journal covers thematic areas such as pre-clinical research, clinical trials, personalized medicine, novel drugs, devices, and biologics, proteomics, genomics, and metabolomics, as well as early phase clinical trial methodology.