Even with recent advances in care, heart failure remains a major cause of morbidity and mortality, which urgently needs new treatments. One of the major antecedents of heart failure is pathological ventricular remodelling, the abnormal change in the size, shape, function or composition of the cardiac ventricles in response to load or injury. Accumulating immune cell subpopulations contribute to the change in cardiac cellular composition that occurs during ventricular remodelling, and these immune cells can facilitate heart failure development. Among cardiac immune cell subpopulations, macrophages that are recognized by their transcriptional or cell-surface expression of the chemokine receptor C-C chemokine receptor type 2 (CCR2), have emerged as playing an especially important role in adverse remodelling. Here, we assimilate the literature that has been generated over the past two decades describing the pathological roles that CCR2+ macrophages play in ventricular remodelling. The goal is to facilitate research and innovation efforts in heart failure therapeutics by drawing attention to the importance of studying the manner by which CCR2+ macrophages mediate their deleterious effects.
Keywords: CCR2; heart failure; inflammation; macrophage; monocyte; myocardial infarction; pressure overload; single-cell RNA sequencing; ventricular remodelling.