Key result
Disrupted cardiac cell-to-cell communication drives inflammation, fibrosis, and dysfunction in chronic heart failure.
Why the study?
A deeper understanding of intercellular communication among cardiomyocytes, fibroblasts, endothelial cells, and macrophages provides insights into the pathogenic pathways of chronic heart failure and lays the foundation for targeted and multi-target therapeutic strategies.
Answers are grounded in this paper and cite their sources.
This review summarizes the intercellular communication mechanisms among cardiomyocytes, fibroblasts, endothelial cells, and macrophages in chronic heart failure to provide theoretical insights for targeted therapeutic strategies.
Chronic heart failure (CHF) is a complex disease syndrome closely linked to the interactions among various cell types. These cells establish dynamic communication networks via mediators such as inflammatory factors, cytokines, and exosomes, which collectively drive the progression of key pathological processes including chronic inflammation, myocardial fibrosis, microcirculatory dysfunction, and myocardial contractile dysfunction. A deeper understanding of these intercellular “conversations” not only provides theoretical insights into the pathogenic pathways of heart failure but also lays the foundation for the development of targeted interventions and multi-target therapeutic strategies. This review focuses on the interactions among critical mediators in CHF, including cardiomyocytes, fibroblasts, endothelial cells, and macrophages, exploring their regulatory mechanisms and biological roles throughout the progression of chronic heart failure, with the aim of offering new perspectives for clinical treatment strategies.
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Xiao et al. (2026) conducted a review in Chronic heart failure. Dysregulated intercellular communication among cardiomyocytes, fibroblasts, endothelial cells, and macrophages drives inflammation, fibrosis, and contractile dysfunction in chronic heart failure.
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