Key result
CKD-driven epicardial adipose tissue dysfunction promotes CVD and serves as a potential therapeutic target.
Why the study?
Epicardial adipose tissue is increasingly implicated as a key contributor to cardiovascular disease in patients with chronic kidney disease.
Epicardial adipose tissue dysfunction driven by CKD-induced metabolic dysregulation and uremic toxins is a key contributor to cardiovascular disease in this population.
Epicardial adipose tissue, a metabolically active visceral fat depot surrounding the heart, is increasingly implicated as a key contributor to cardiovascular disease in patients with chronic kidney disease. This review explores how chronic kidney disease induced metabolic dysregulation, chronic inflammation and uremic toxin accumulation lead to epicardial adipose tissue dysfunction. Pathologically altered epicardial adipose tissue promotes atherosclerosis, myocardial fibrosis and arrhythmogenesis through paracrine signaling, oxidative stress and direct cellular interactions. Advanced imaging modalities now enable precise epicardial adipose tissue quantification, revealing its correlation with cardiovascular outcomes in chronic kidney disease. Epicardial adipose tissue is expected to become a new target for predicting and assessing cardiovascular risk, and for interventions to reduce cardiovascular risk in chronic kidney disease patients, thereby providing a new direciovascular risk, and for interventions to reduce cardiovascular risk in chronic kidney disease patients, thereby providing a new direction for future risk management and therapeutic strategies.
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Cui et al. (2025) conducted a review in Chronic kidney disease and cardiovascular disease. Epicardial adipose tissue was evaluated. Epicardial adipose tissue dysfunction, driven by chronic kidney disease-induced metabolic dysregulation and inflammation, promotes cardiovascular disease and serves as a potential therapeutic target.
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