Key result
Mitochondrial metabolic alterations drive HF pathophysiology and emerge as potential therapeutic targets.
Why the study?
Heart failure prevalence is growing despite treatment progress, and the role of mitochondrial metabolic remodeling in HF pathophysiology extends beyond energy deficiency.
This review highlights metabolic alterations in mitochondria and discusses potential metabolic approaches to improve cardiac function in heart failure.
Mitochondrial targets merit exploration in HF trials; leaves open whether metabolic modulation will improve clinical outcomes.
Despite considerable progress in treating cardiac disorders, the prevalence of heart failure (HF) keeps growing, making it a global medical and economic burden. HF is characterized by profound metabolic remodeling, which mostly occurs in the mitochondria. Although it is well established that the failing heart is energy-deficient, the role of mitochondria in the pathophysiology of HF extends beyond the energetic aspects. Changes in substrate oxidation, tricarboxylic acid cycle and the respiratory chain have emerged as key players in regulating myocardial energy homeostasis, Ca2+ handling, oxidative stress and inflammation. This work aims to highlight metabolic alterations in the mitochondria and their far-reaching effects on the pathophysiology of HF. Based on this knowledge, we will also discuss potential metabolic approaches to improve cardiac function.
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Schenkl et al. (2023) conducted a review in Heart failure. Metabolic approaches targeting mitochondrial metabolism was evaluated. Mitochondrial metabolic alterations, including changes in substrate oxidation and the respiratory chain, play a key role in heart failure pathophysiology and represent potential therapeutic targets.
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