Key result
Targeting impaired energy provision and metabolic remodeling offers a potential strategy to optimize HF management.
Why the study?
Despite ongoing therapeutic developments, great gaps remain in understanding heart failure, with high morbidity and readmission rates persisting.
Targeting impaired energy provision and improving the cellular environment represents a potential therapeutic strategy for optimizing heart failure management.
Should not yet change HF practice; leaves open validation of metabolic targets in prospective trials.
Heart Failure (HF) has been one of the leading causes of death worldwide. Though its latent mechanism and therapeutic manipulation are updated and developed ceaselessly, there remain great gaps in the cognition of heart failure. High morbidity and readmission rates among HF patients are waiting to be addressed. Recent studies have found that myocardial energy metabolism was closely related to heart failure, in which substrate utilization, as well as intermediate metabolism disorders, insulin resistance, oxidative stress, and mitochondrial dysfunction, might underlie systolic dysfunction and progression of HF. This article centers on the changes and counteraction of cardiac energy metabolism in the failing heart. Therefore, targeting impaired energy provision is of great potential in the treatment of HF. And shifting the objective from traditional neurohormones to improving the cellular environment is expected to further optimize the management of HF.
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Fan et al. (2023) conducted a review in Heart Failure. Targeting impaired energy provision was evaluated. Targeting impaired energy provision and metabolic remodeling offers a potential therapeutic strategy to improve the cellular environment and optimize heart failure management.
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