Key result
Targeting the macrophage autophagy-metabolism axis shifts inflammatory phenotypes to reparative states for post-MI cardiac repair.
Why the study?
Preventing heart failure after myocardial infarction remains challenging, and the integrated role of the macrophage autophagy-metabolism axis in post-MI repair is not fully systematized.
This review highlights the therapeutic potential of targeting the macrophage autophagy-metabolism axis to optimize cardiac repair and prevent heart failure after myocardial infarction.
Suggests mitophagy modulation to prevent post-MI heart failure; extends macrophage mechanisms to first RCT evidence.
Myocardial infarction (MI) is a life-threatening cardiovascular event, and preventing subsequent heart failure remains a major clinical challenge despite available treatments. The repair outcome critically depends on the cardiac immune microenvironment, where macrophages play a pivotal role. Their functional switch from pro-inflammatory to reparative phenotypes is driven by mitochondrial metabolic reprogramming, a process regulated by autophagy, particularly mitophagy. However, the integrated role of the macrophage autophagy-metabolism axis in post-MI repair is not fully systematized. This review comprehensively examines the interplay between macrophage autophagy and mitochondrial metabolic reprogramming. It details how mitophagy maintains mitochondrial fitness to suppress inflammation and fuel the oxidative metabolism essential for reparative macrophage function. The discussion extends to advanced regulatory mechanisms, including inter-organelle communication, mechanosensing, and intercellular mitochondrial transfer. Furthermore, the review evaluates emerging therapeutic strategies, such as precision nanomedicine and multi-target interventions, within complex clinical contexts like diabetic MI. Key challenges, including the spatiotemporal complexity of macrophage dynamics and translational bottlenecks, are also addressed. By synthesizing current insights, this review establishes a novel immunometabolic framework centered on the macrophage autophagy-metabolism axis. It highlights that targeting this axis holds significant therapeutic potential for optimizing cardiac repair. The review provides forward-looking perspectives, emphasizing the need for intelligent, spatiotemporally precise therapeutic platforms to advance the development of targeted therapies for MI. Elucidates how macrophage mitophagy orchestrates immunometabolic switching between inflammatory and reparative phenotypes post-myocardial infarction, offering novel therapeutic targets. Explores novel regulatory dimensions including inter-organelle communication and mechanobiology, providing fresh perspectives on microenvironmental control of macrophage function. Evaluates cutting-edge therapeutic strategies like precision nanomedicine and multi-target interventions, highlighting translational potential in complex clinical scenarios. Synthesizes the macrophage autophagy-metabolism axis as an integrated framework, paving the way for next-generation cardiac repair therapies.
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Zhang et al. (2026) conducted a review in Myocardial infarction. Modulation of macrophage autophagy and mitochondrial metabolic reprogramming was evaluated. Targeting the macrophage autophagy-metabolism axis orchestrates the switch between inflammatory and reparative phenotypes, offering a novel framework for post-myocardial infarction cardiac repair.
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