Review: Cellular Senescence and SASP in Heart Failure With Preserved Ejection Fraction
This review assesses evidence linking cellular senescence and the senescence-associated secretory phenotype (SASP) to heart failure with preserved ejection fraction (HFpEF), and weighs the therapeutic potential and limits of senolytics and senomorphics. Much of the evidence is preclinical or associative, and HFpEF-specific human data remain limited. [1]
Automatic summary · not editorially reviewed
The key findings
HFpEF accounts for nearly 50% of global heart failure cases and remains a major clinical challenge. [1]
HFpEF is increasingly recognized as a heterogeneous multisystem syndrome closely associated with aging, cardiometabolic comorbidities and chronic low-grade inflammation. [1]
Much of the evidence linking senescence to HFpEF remains preclinical or associative, and HFpEF-specific human data are still limited. [1]
The source at a glance
- Study type / format
- Review (abstract only)
- Population / context
- People with heart failure with preserved ejection fraction (HFpEF), described in a review; no specific study sample reported in the abstract.
- Summary based on
- Study abstract
- Original publication
- October 12, 2026
HFpEF as a heterogeneous aging-linked syndrome
The review frames HFpEF as a major clinical challenge: it accounts for nearly 50% of global heart failure cases and is marked by heterogeneous pathophysiology, substantial residual morbidity and limited mechanism-based treatment options. HFpEF is increasingly recognized as a heterogeneous multisystem syndrome closely associated with aging, cardiometabolic comorbidities and chronic low-grade inflammation. The review asks whether cellular senescence and SASP could link several of these systemic stressors to cardiovascular dysfunction.
Supporting source [1]
SASP circuit and context-dependent senescence effects
According to the review, SASP may act through paracrine and endocrine communication and create a self-reinforcing circuit in the myocardium. At the same time, the biological consequences of cellular senescence are described as highly context-, cell type- and stage-dependent. Transient senescence may exert adaptive or tissue-protective effects under certain conditions. These points mean senescence is not presented as uniformly harmful.
Supporting source [1]
Senolytics and senomorphics: potential and evidence limits
The review examines the therapeutic potential and limitations of senolytics and senomorphics for HFpEF. It states that much of the current evidence linking senescence to HFpEF remains preclinical or associative, and that HFpEF-specific human data are still limited. The review therefore assesses the evidence rather than establishing that targeting senescence benefits people with HFpEF.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. The source itself notes that much evidence is preclinical or associative and that HFpEF-specific human data are limited. Associations do not establish causation, and preclinical findings do not show human benefit.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Wang J, Liu R, Zhang X, Qi G, Xu Q, Jia F. · europepmc.org · October 12, 2026