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Abstract
Heart failure with preserved ejection fraction (HFpEF) is strongly associated with aging and characterized by diastolic dysfunction and chronic low-grade inflammation.
- Cellular senescence and the senescence-associated secretory phenotype (SASP) may play significant roles in the development and progression of HFpEF.
- SASP factors are linked to myocardial fibrosis, microvascular dysfunction, and damage to heart muscle cells.
- Evidence from preclinical and clinical studies suggests that targeting SASP pathways could offer therapeutic potential for HFpEF.
- Senolytic agents that eliminate senescent cells and senomorphic compounds that inhibit SASP factor secretion are being evaluated as treatment options.
- Key translational challenges include limited tissue specificity for delivering senolytic treatments and a lack of reliable biomarkers for monitoring SASP in therapy.
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