Cardiac macrophages and emerging roles for their metabolism after myocardial infarction.
Cardiac macrophages and emerging roles for their metabolism after myocardial infarction.
复制标题
DOI：
10.1172/jci171953
复制
发表时间：
2023-09-15
期刊：
影响因子：
--
通讯作者：
Thorp EB
中科院分区：
文献类型：
--
作者：
Thorp EB
对心脏免疫学的兴趣达到了新的高度，因为实验心脏病学领域致力于挖掘免疫治疗在临床护理中的未实现的潜力。在这个空间中是心脏巨噬细胞，它是健康和疾病中心脏功能的关键调节剂。心肌梗死后，骨髓巨噬细胞既保护心脏又损害心脏。在不同程度上，这些结果是髓系个体发生和异质性以及功能性细胞可塑性的功能。细胞外环境进一步塑造了多样性，冠状动脉闭塞后细胞外环境波动很大。营养物质的缺血限制限制了免疫细胞的代谢潜力，越来越多的证据支持巨噬细胞代谢与不同炎症后果相结合的范式，尽管这在心脏中的实验证据刚刚出现。在此，我们研究了缺血损伤后的异质心脏巨噬细胞反应，重点关注免疫代谢的推定贡献以及治疗相关心脏损伤与心脏修复的意义。
Interest in cardioimmunology has reached new heights as the experimental cardiology field works to tap the unrealized potential of immunotherapy for clinical care. Within this space is the cardiac macrophage, a key modulator of cardiac function in health and disease. After a myocardial infarction, myeloid macrophages both protect and harm the heart. To varying degrees, such outcomes are a function of myeloid ontogeny and heterogeneity, as well as functional cellular plasticity. Diversity is further shaped by the extracellular milieu, which fluctuates considerably after coronary occlusion. Ischemic limitation of nutrients constrains the metabolic potential of immune cells, and accumulating evidence supports a paradigm whereby macrophage metabolism is coupled to divergent inflammatory consequences, although experimental evidence for this in the heart is just emerging. Herein we examine the heterogeneous cardiac macrophage response following ischemic injury, with a focus on integrating putative contributions of immunometabolism and implications for therapeutically relevant cardiac injury versus cardiac repair.