Key result
Cardiac macrophages play essential roles in maintaining heart homeostasis through phagocytosis and electrical conduction, but also contribute to adverse cardiac remodeling and heart failure progression.
Why the study?
Studies on detailed mechanisms of cardiac macrophage function are still in progress and could enable potential therapeutic applications in heart homeostasis and failure.
Understanding the diverse origins and functions of cardiac macrophages provides insights into their dual roles in cardiac homeostasis and heart failure pathogenesis, highlighting their potential as therapeutic targets.
May inform macrophage-targeted HF therapies; leaves open clinical translation pending interventional trials.
Macrophages are essential components of the immune system and play a role in the normal functioning of the cardiovascular system. Depending on their origin and phenotype, cardiac macrophages perform various functions. In a steady-state, these cells play a beneficial role in maintaining cardiac homeostasis by defending the body from pathogens and eliminating apoptotic cells, participating in electrical conduction, vessel patrolling, and arterial tone regulation. However, macrophages also take part in adverse cardiac remodeling that could lead to the development and progression of heart failure (HF) in such HF comorbidities as hypertension, obesity, diabetes, and myocardial infarction. Nevertheless, studies on detailed mechanisms of cardiac macrophage function are still in progress, and could enable potential therapeutic applications of these cells. This review aims to present the latest reports on the origin, heterogeneity, and functions of cardiac macrophages in the healthy heart and in cardiovascular diseases leading to HF. The potential therapeutic use of macrophages is also briefly discussed.
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Moskalik et al. (2021) conducted a review in Heart failure and cardiovascular diseases. Cardiac macrophages play essential roles in maintaining heart homeostasis through phagocytosis and electrical conduction, but also contribute to adverse cardiac remodeling and heart failure progression.
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