Observational analysis reveals neutrophil elastase's role in diastolic dysfunction in HFpEF, indicating a potential therapeutic target.
Key Points
Neutrophil elastase deficiency alleviated diastolic dysfunction in mice with heart failure, indicating its critical role in HFpEF.
Mice undergoing the 'Two-hit' protocol developed significant diastolic dysfunctions, demonstrated by higher left ventricular filling pressure and worsened exercise performance.
Assessment using pharmacologic inhibitors and gene transfer provided insights into the NE-RBPMS-Titin signaling pathway's effect on cardiac dysfunction.
Identifying RBPMS as a target opens avenues for potential therapies aimed at ameliorating heart failure symptoms associated with preserved ejection fraction.