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A novel paradigm for heart failure with preserved ejection fraction: comorbidities drive myocardial dysfunction and remodeling through coronary microvascular endothelial inflammation

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The pathological mechanism might be the dysregulation of glucose metabolism, which triggered the accumulation of epicardial adipose tissue (EAT) and free fatty acids in heart, leading to myocardial lipotoxicity, oxidative stress, and mitochondrial dysfunction [41]

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