Key result
Impaired fatty acid oxidation in HFpEF suppresses mitophagy, while enhancing fatty acid oxidation via ACC2 deficiency or stimulating mitophagy pharmacologically improves cardiac function in preclinical models.
Why the study?
Does enhancing fatty acid oxidation or mitophagy improve mitochondrial energetics and diastolic function in preclinical models of HFpEF?
Does enhancing fatty acid oxidation or mitophagy improve mitochondrial energetics and diastolic function in preclinical models of HFpEF?
This editorial highlights preclinical evidence that impaired fatty acid oxidation blunts mitophagy in HFpEF, and restoring this pathway through ACC2 inhibition or mitophagy activators could represent a novel therapeutic strategy.
Heart failure with preserved ejection fraction (HFpEF) accounts for nearly half of all heart failure cases and represents a significant global health burden with increasing prevalence 1, 2 .HFpEF presents with symptoms and signs of heart failure, including reduced exercise capacity, myocardial stiffness, and elevated left ventricular filling pressure, despite normal or near normal LV ejection fraction (LVEF; ≥50 percent) 1, 2 .It is frequently associated with comorbidities such as diabetes mellitus, obesity, atrial fibrillation and renal dysfunction 1, 2 .However, the complex pathophysiology of HFpEF and diverse presentation observed in patients pose challenges for both diagnosis and development of effective therapies.Hence, a deeper understanding of its underlying molecular mechanisms of HFpEF is urgently needed.
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Fang et al. (2024) conducted an editorial in Heart failure with preserved ejection fraction (HFpEF). ACC2 inhibition or mitophagy activation was evaluated. Impaired fatty acid oxidation in HFpEF suppresses mitophagy, while enhancing fatty acid oxidation via ACC2 deficiency or stimulating mitophagy pharmacologically improves cardiac function in preclinical models.
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