Cardiac macrophages and emerging roles for their metabolism after myocardial infarction

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.

Automated summary

Interest in cardioimmunology has grown as researchers explore the potential of immunotherapy for clinical care. The role of cardiac macrophages, which modulate cardiac function, has become a focus of study. After a heart attack, myeloid macrophages can both protect and harm the heart. The outcomes depend on factors such as myeloid ontogeny, heterogeneity, and cellular plasticity. The extracellular milieu and nutrient limitations also play a role.