Inhibition of differentiation of monocyte-derived macrophages toward an M2-Like phenotype May Be a neglected mechanism of β-AR receptor blocker therapy for atherosclerosis

TL;DR

This paper suggests that beta-blockers may help treat atherosclerosis by preventing macrophages from becoming M2-like, which could reduce plaque formation.

Contribution

The paper proposes a novel mechanism for beta-blockers' efficacy in atherosclerosis by linking them to inhibition of M2 macrophage differentiation.

Findings

Beta-AR blockers may stabilize atherosclerotic plaques by inhibiting M2-like macrophage differentiation.

Lipid-induced macrophage polarization plays a role in atherosclerosis progression.

Current evidence supports the use of beta-blockers for treating atherosclerosis.

Abstract

The clinical efficacy of adrenergic β-receptor (β-AR) blockers in significantly stabilizing atherosclerotic plaques has been extensively supported by evidence-based medical research; however, the underlying mechanism remains unclear. Recent findings have highlighted the impact of lipid-induced aberrant polarization of macrophages during normal inflammatory-repair and regenerative processes on atherosclerosis formation and progression. In this review, we explore the relationship between macrophage polarization and atherosclerosis, as well as the influence of β-AR blockers on macrophage polarization. Based on the robust evidence supporting the use of β-AR blockers for treating atherosclerosis, we propose that their main mechanism involves inhibiting monocyte-derived macrophage differentiation towards an M2-like phenotype.

Figures