Multiple roles of cardiac macrophages in heart homeostasis and failure

Abstract

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.

Dirty Jobs: Macrophages at the Heart of Cardiovascular Disease

“…This role is carried out through inflammatory mediation by M1 and M2 macrophages, the recruitment of inflammatory cytokines and neutrophils, as well as the repair and remodeling of cardiac tissue [ 11 , 13 ]. The exact roles of macrophages during heart failure are not entirely known; however, different pathways have been observed based on the form of heart failure that is present [ 38 , 39 ]. Heart failure is typically classified into three forms: heart failure with a preserved ejection fraction (HFpEF), heart failure with a reduced ejection fraction (HFrEF), and heart failure with a mid-range ejection fraction (HFmrEF) [ 39 , 40 ].…”

New insights into the pathogenesis of cardiac papillary fibroelastomas

“…This process can be modulated by endothelial and stromal cells such as fibroblasts and macrophages and attributed to elevated levels of monocyte chemoattractant protein-1 [52][53][54][55][56]. Other research reported that bone marrow-derived macrophages can transdifferentiate into collagen-producing α SMA + myofibroblasts via TGF-β/Smad3 signaling through macrophage to myofibroblast transition during renal fibrosis [57][58][59]. Additionally, Haider et al used myeloid specific cre reporter mice LysM(Cre /+ ; ROSA26(EYFP /+ )) demonstrated that macrophages can transdifferentiate into fibroblast-like cells in the post-myocardial infarction heart [60].…”

Role of Distinct Macrophage Populations in the Development of Heart Failure in Macrophage Activation Syndrome

“…We can distinguish three major types of heart failure, based on the left ventricular ejection fraction (LVEF) parameter: heart failure with a preserved ejection fraction (HFpEF), characterized by LVEF over 50%, heart failure with a reduced ejection fraction (HFrEF) with LVEF below 40%, and the intermediate heart failure with a mid-range ejection fraction (HFmrEF). These conditions differ in both their triggering factors and their development mechanisms [ 86 , 87 , 88 ]—particularly types of autoimmune response and the resulting restructuring of extracellular space [ 89 ].…”