Key result
Immune cells mediate both the inflammatory clearance of dead cells and subsequent fibrogenic responses during the repair and remodeling of the infarcted myocardium.
Understanding and modulating immune cell phenotypes post-myocardial infarction represents a potential therapeutic avenue to prevent adverse remodeling and promote myocardial regeneration.
Immune modulation post-MI should not yet change practice; leaves open phenotype-specific targeting to limit remodeling.
The immune system plays a critical role in both repair and remodeling of the infarcted myocardium. Danger signals released by dying cardiomyocytes mobilize, recruit, and activate immune cells, triggering an inflammatory reaction. CXC chemokines containing the ELR motif attract neutrophils, while CC chemokines mediate recruitment of mononuclear cell subpopulations, contributing to clearance of the infarct from dead cells and matrix debris. Immune cell subsets also participate in suppression and containment of the postinfarction inflammatory response by secreting anti-inflammatory mediators, such as IL-10 and TGF-β. As proinflammatory signaling is suppressed, macrophage subpopulations, mast cells and lymphocytes, activate fibrogenic and angiogenic responses, contributing to scar formation. In the viable remodeling myocardium, chronic activation of immune cells may promote fibrosis and hypertrophy. This review discusses the role of immune cells in repair and remodeling of the infarcted myocardium. Understanding the role of immune cells in myocardial infarction is critical for the development of therapeutic strategies aimed at protecting the infarcted heart from adverse remodeling. Moreover, modulation of immune cell phenotype may be required in order to achieve the visionary goal of myocardial regeneration.
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Chen et al. (2016) conducted a review in Myocardial infarction. Immune cells mediate both the inflammatory clearance of dead cells and subsequent fibrogenic responses during the repair and remodeling of the infarcted myocardium.
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