Key result
Myocardial lipid accumulation and lipotoxicity drive the initiation and progression of human diabetic cardiomyopathy.
Why the study?
Despite extensive preclinical models of hyperglycemia and insulin resistance, evidence regarding pathogenic and histological alterations of diabetic cardiomyopathy remains poorly understood in humans.
This review synthesizes current evidence on human diabetic cardiomyopathy, emphasizing the role of lipotoxicity, insulin resistance, and progressive fibrosis in its pathogenesis.
Does not change diabetic cardiomyopathy management; leaves open whether targeting lipotoxicity improves outcomes.
Growing interest has been accumulated in the definition of worsening effects of diabetes in the cardiovascular system. This is associated with epidemiological data regarding the high incidence of heart failure (HF) in diabetic patients. To investigate the detrimental effects both of hyperglycemia and insulin resistance, a lot of preclinical models were developed. However, the evidence of pathogenic and histological alterations of the so-called diabetic cardiomyopathy (DCM) is still poorly understood in humans. Here, we provide a stringent literature analysis to investigate unique data regarding human DCM. This approach established that lipotoxic-related events might play a central role in the initiation and progression of human DCM. The major limitation in the acquisition of human data is due to the fact of heart specimen availability. Postmortem analysis revealed the end stage of the disease; thus, we need to gain knowledge on the pathogenic events from the early stages until cardiac fibrosis underlying the end-stage HF.
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Marfella et al. (2021) conducted a review in Diabetic cardiomyopathy. Lipotoxic-related events and myocardial lipid accumulation play a central role in the initiation and progression of human diabetic cardiomyopathy.
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