Cardiac Macrophages — Keeping the Engine Running Clean

This article explores the essential role of cardiac-resident macrophages (cMacs) in maintaining myocardial homeostasis. Referencing a recent study by Nicolás-Ávila et al., it describes how macrophages scavenge spent mitochondria emitted by cardiomyocytes in structures called exophers an ATP-intensive, phosphatidylserine-tagged process facilitated by the efferocytosis receptor MerTK. In mice, depletion of cMacs or disruption of MerTK led to mitochondrial dysfunction, impaired ATP production, and echocardiographic signs of heart failure with preserved ejection fraction. The article notes that unlike other organs, the heart relies heavily on this mitochondrial transfer mechanism. Similar scavenging may occur in high-energy tissues like skeletal muscle and retina. The discussion suggests potential biomarker utility of soluble MerTK post–myocardial infarction, and proposes MerTK-targeted strategies as future cardioprotective interventions.

This article explores the essential role of cardiac-resident macrophages (cMacs) in maintaining myocardial homeostasis. Referencing a recent study by Nicolás-Ávila et al., it describes how macrophages scavenge spent mitochondria emitted by cardiomyocytes in structures called exophers an ATP-intensive, phosphatidylserine-tagged process facilitated by the efferocytosis receptor MerTK. In mice, depletion of cMacs or disruption of MerTK led to mitochondrial dysfunction, impaired ATP production, and echocardiographic signs of heart failure with preserved ejection fraction. The article notes that unlike other organs, the heart relies heavily on this mitochondrial transfer mechanism. Similar scavenging may occur in high-energy tissues like skeletal muscle and retina. The discussion suggests potential biomarker utility of soluble MerTK post–myocardial infarction, and proposes MerTK-targeted strategies as future cardioprotective interventions.