Macrophage-Dependent Intercellular Crosstalk in Multiphenotypic Heart Failure With Preserved Ejection Fraction.

Area of Science:

• Cardiology
• Immunology
• Metabolic Syndrome

Background:

• Heart failure with preserved ejection fraction (HFpEF) is a complex syndrome, not a single disease.
• Cardiac macrophages are key immune cells involved in HFpEF pathogenesis.
• HFpEF involves inflammation and metabolic dysregulation.

Purpose of the Study:

• To review the role of cardiac macrophages in HFpEF.
• To explore the heterogeneity of cardiac macrophages and HFpEF phenotypes.
• To synthesize evidence on how risk factors reprogram macrophages in HFpEF.

Main Methods:

• Literature review synthesizing preclinical and clinical evidence.
• Analysis of macrophage heterogeneity and phenotypic switching.
• Examination of macrophage interactions with other cardiac cells.

Main Results:

• Risk factors like aging and hypertension reprogram cardiac macrophages.
• Reprogrammed macrophages promote inflammation, fibrosis, and endothelial dysfunction.
• Macrophage-driven crosstalk exacerbates maladaptive cardiac remodeling.

Conclusions:

• Cardiac macrophages orchestrate a vicious cycle in HFpEF.
• Targeting specific macrophage subsets offers a potential therapeutic strategy for HFpEF.
• Addressing macrophage dysfunction is crucial for managing this heterogeneous syndrome.