Key result
Skeletal muscle SIRT3 modulates pulmonary vascular remodeling in PH-HFpEF via novel endocrine signaling.
Why the study?
Pulmonary hypertension is a major complication in HFpEF with no specific therapies for PH associated with HFpEF, motivating investigation of skeletal muscle SIRT3's role.
Skeletal muscle SIRT3 may represent a novel endocrine signaling pathway involved in pulmonary vascular remodeling in PH-HFpEF, presenting a potential future therapeutic target.
Pulmonary hypertension (PH) is a major complication linked to adverse outcomes in heart failure with preserved ejection fraction (HFpEF), yet no specific therapies exist for PH associated with HFpEF (PH-HFpEF). We have recently reported on the role of skeletal muscle SIRT3 (sirtuin-3) in modulation of PH-HFpEF, suggesting a novel endocrine signaling pathway for skeletal muscle modulation of pulmonary vascular remodeling.
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Jheng et al. (2024) studied Pulmonary hypertension associated with heart failure with preserved ejection fraction (PH-HFpEF). Skeletal muscle SIRT3 deficiency was evaluated. Skeletal muscle SIRT3 plays a role in the modulation of pulmonary vascular remodeling in PH-HFpEF, suggesting a novel endocrine signaling pathway.
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