Abstract Cardiovascular diseases (CVDs) account for millions of deaths worldwide each year, underlining their significant impact on global health. An expanding body of evidence identifies atherosclerosis, myocardial infarction, heart failure, and ischemic stroke as major contributors to this burden. Central to the pathogenesis of these conditions is the inflammatory response—a key defense mechanism that, when dysregulated, accelerates disease progression and disrupts cellular homeostasis, ultimately leading to adverse clinical outcomes. Efficient resolution of inflammation is essential not only for halting the inflammatory responses but also for restoring tissue integrity. One critical aspect of resolving inflammation is the efficient clearance of apoptotic cells, a process known as “efferocytosis,” which remains underappreciated. Cardiac macrophages are tasked with removing apoptotic cells, necrotic cells, and cellular debris through efferocytosis. Importantly, recent studies have demonstrated that efficient efferocytosis is associated with improved outcomes in CVDs, whereas impaired efferocytosis perpetuates inflammation and hinders recovery. This tightly regulated mechanism not only resolves inflammation by suppressing proinflammatory cytokines but also stimulates the production of anti-inflammatory cytokines and reprograms macrophages to promote tissue homeostasis. This mini-review consolidates current understanding of macrophage efferocytosis and its molecular mechanisms, providing valuable insights into cardiac health and highlighting its significant potential as a therapeutic avenue for treating CVDs.
Gupta et al. (Sun,) studied this question.