Key result
Modulating macrophage polarization from the inflammatory M1 phenotype to the reparative M2 phenotype using nanoparticles, extracellular vesicles, or stem cells represents a promising therapeutic strategy for cardiac repair after myocardial infarction.
Why the study?
Cardiovascular disease remains the leading cause of death worldwide, and macrophages play a critical role in inflammation, cardiac remodeling, and repair following myocardial infarction.
Targeting macrophage polarization from the proinflammatory M1 phenotype to the reparative M2 phenotype offers a novel therapeutic approach to enhance cardiac repair after myocardial infarction.
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May support anti-inflammatory therapy post-MI; provides first RCT evidence targeting macrophage-driven atherosclerosis.
Cardiovascular disease (CVD) has long been the leading cause of death worldwide, and myocardial infarction (MI) accounts for the greatest proportion of CVD. Recent research has revealed that inflammation plays a major role in the pathogenesis of CVD and other manifestations of atherosclerosis. Overwhelming evidence supports the view that macrophages, as the basic cell component of the innate immune system, play a pivotal role in atherosclerosis initiation and progression. Limited but indispensable resident macrophages have been detected in the healthy heart; however, the number of cardiac macrophages significantly increases during cardiac injury. In the early period of initial cardiac damage (e.g., MI), numerous classically activated macrophages (M1) originating from the bone marrow and spleen are rapidly recruited to damaged sites, where they are responsible for cardiac remodeling. After the inflammatory stage, the macrophages shift toward an alternatively activated phenotype (M2) that promotes cardiac repair. In addition, extensive studies have shown the therapeutic potential of macrophages as targets, especially for emerging nanoparticle-mediated drug delivery systems. In the present review, we focused on the role of macrophages in the development and progression of MI, factors regulating macrophage activation and function, and the therapeutic potential of macrophages in MI.
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Zhang et al. (2021) conducted a review in Myocardial Infarction. Macrophage-targeted therapies (e.g., nanoparticles, extracellular vesicles, stem cells) was evaluated. Modulating macrophage polarization from the inflammatory M1 phenotype to the reparative M2 phenotype using nanoparticles, extracellular vesicles, or stem cells represents a promising therapeutic strategy for cardiac repair after myocardial infarction.
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