Emerging roles of macrophages in heart failure and associated treatment approaches

Abstract

Heart failure is typically caused by different cardiovascular conditions and has a poor prognosis. Despite the advances in treatment in recent decades, heart failure has remained a major cause of morbidity and mortality worldwide. As revealed by in vivo and in vitro experiments, inflammation plays a crucial role in adverse cardiac remodeling, ultimately leading to heart failure. Macrophages are central to the innate immune system, and they are the most indispensable cell type for all cardiac injuries and remodeling stages. The immediate microenvironment regulates their polarization and secretion. In this review, we summarize the phenotypic heterogeneity and governing roles of macrophages in the infarcted, inflamed, and aging heart and assess their significance as potential therapeutic targets in heart failure. We also highlight the current missing links and major challenges in the field that remain to be addressed before macrophages can be exploited for therapeutic applications.

Effects of vitamin D signaling in cardiovascular disease: centrality of macrophage polarization

“…The central actors in maintaining tissue homeostasis are macrophages (29,30), dendritic cells (31,32), stem cells (33), and vitamin D (34)(35)(36)(37)(38). However, our understanding of their interaction remains incomplete, as evidenced by multiple inconclusive clinical trials seeking to halt the progression of cardiovascular disease associated with vitamin D deficiency (39)(40)(41)(42)(43).…”