Key result
Reprogramming macrophage metabolism emerges as a promising immunotherapy to enhance post-MI cardiac repair.
Why the study?
Macrophage polarization is directed by immunometabolic reprogramming after myocardial infarction, but the metabolic circuits connecting immune function to durable cardiac recovery remain incompletely defined.
This review highlights the metabolic pathways governing macrophage polarization after myocardial infarction and identifies potential therapeutic targets for improving cardiac repair and limiting heart failure progression.
May support macrophage metabolic targeting post-MI; leaves open clinical translation pending prospective trials.
Background Myocardial infarction (MI) elicits a tightly staged immune response in which macrophages coordinate early inflammation, subsequent tissue repair, and long-term ventricular remodeling. Growing evidence indicates that macrophage polarization is directed by immunometabolic reprogramming; however, the metabolic circuits that connect immune function to durable cardiac recovery remain incompletely defined. Content This review integrates current insights into the spatiotemporal, metabolic, and functional regulation of macrophages after MI. We summarize how glucose metabolism (glycolysis and the pentose phosphate pathway), TCA cycle rewiring and immunometabolic intermediates, lipid and amino-acid metabolism, iron handling and ferroptosis, purinergic and NAD⁺-dependent signaling, oxidative stress pathways, and vitamin-dependent regulation shape inflammatory versus reparative macrophage states. We highlight drug-targetable mediators—including lactate, succinate, α-KG, itaconate, kynurenine, and NAD⁺-linked pathways—and discuss how stage-specific targeting may suppress early injurious inflammation while promoting reparative remodeling. We also review advances in nanotechnology- and exosome-based delivery platforms that enable cardiac macrophage–directed interventions. Outlook Clinical translation will require deeper characterization of human macrophage heterogeneity, development of in vivo metabolic biomarkers, and validation in prospective multi-omics–anchored human studies. Temporally controlled combination therapies coupled with precision delivery systems may maximize cardiac repair while minimizing systemic metabolic toxicity. Conclusions Macrophage immunometabolism is a central determinant of post-MI healing and remodeling. Therapeutic reprogramming of macrophage metabolism represents a promising precision-immunotherapy strategy to improve repair, limit heart failure progression, and expand future cardiovascular treatment options. Clinical trial number Not applicable.
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Zhou et al. (2026) conducted a review in Myocardial infarction. Metabolic reprogramming of macrophages was evaluated. Therapeutic reprogramming of macrophage metabolism represents a promising precision-immunotherapy strategy to improve cardiac repair and limit heart failure progression after myocardial infarction.
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