Key result
Mitochondrial dysfunction contributes to impaired oxygen utilization and exercise intolerance in HFpEF.
Why the study?
Mitochondrial abnormalities can significantly contribute to impaired oxygen utilization and exercise intolerance in HFpEF, but the evidence, assessment methods, and therapeutic potential require synthesis.
Design
Review
Authors
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Supports mitochondrial-targeted therapies as research priority in HFpEF; leaves open whether interventions improve exercise capacity or outcomes.
Mitochondrial dysfunction contributes to exercise intolerance in HFpEF and represents a potential therapeutic target.
Kumar et al. (2019) studied this question. Mitochondrial dysfunction significantly contributes to impaired oxygen utilization and exercise intolerance in patients with heart failure with preserved ejection fraction (HFpEF).
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