Key result
Cardiac lipotoxicity, driven by PPAR-α inhibition, β-adrenergic receptor desensitization, and mitochondrial dysfunction, contributes to the aggravation of cardiac function in age-related cardiomyopathy.
Understanding the mechanisms of lipid-driven age-related cardiomyopathy may reveal novel therapeutic targets for cardiac aging.
No immediate practice change in elderly HF; leaves open lipotoxicity-targeted therapies for prospective validation.
Age-related cardiomyopathy accounts for a significant part of heart failure cases. Imbalance of the energetic equilibrium of the heart along with mitochondrial dysfunction and impaired β-adrenergic receptor signaling contributes in the aggravation of cardiac function in the elderly. In this review article, studies that correlate cardiac aging with lipotoxicity are summarized. The involvement of inhibition of peroxisome proliferator-activated receptor-α, β-adrenergic receptor desensitization, and mitochondrial dysfunction as underlying mechanisms for the lipid-driven age-related cardiomyopathy are presented with the aim to indicate potential therapeutic targets for cardiac aging.
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Konstantinos Drosatos (2016) conducted a review in Age-related cardiomyopathy. Cardiac lipotoxicity was evaluated. Cardiac lipotoxicity, driven by PPAR-α inhibition, β-adrenergic receptor desensitization, and mitochondrial dysfunction, contributes to the aggravation of cardiac function in age-related cardiomyopathy.
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