Research update: long-term senolytic treatment and exercise in the ageing mouse heart

Research update · October 2026 · Summarises a published peer-reviewed study for educational purposes.

The paper

Bevington RT, Johnson AL, Hockey BL, Fajardo VA, Parise G. Chronic senolytic treatment and/or aerobic exercise reduce senescence and improve myocardial function during aging in the heart. Aging Cell. 2026;25(10):e70759. Open access.
PubMed: https://pubmed.ncbi.nlm.nih.gov/42841582/ · DOI: https://doi.org/10.1111/acel.70759 · Full text: https://pmc.ncbi.nlm.nih.gov/articles/PMC13644388/

At a glance

Why the study was done

Senescent cells have been reported to accumulate in the heart with age, both in cardiomyocytes (heart muscle cells) and in interstitial cells. Earlier studies had examined senolytic compounds and exercise separately, but mostly over short periods. The authors asked two questions: whether either approach, applied long-term from middle age, would change senescence markers in the mouse heart, and whether combining them would have an additive effect [1].

What the authors reported

• In all three intervention groups (D+Q, exercise, and both combined), the proportion of heart cells positive for p16, p21 and γ-H2AX was lower than in the naturally aged control mice.
• The intervention groups also showed differences in several ultrasound measures of heart function, including measures of diastolic (filling) function, compared with the aged controls.
• No additive effect was seen: the combined group did not differ meaningfully from either intervention alone. The authors suggest that each approach may already have reduced the pool of senescent cells, leaving little room for an extra effect.
• At the whole-heart level, p16 and p21 protein increased with age, but neither these nor the SASP markers measured were altered by any intervention.
• Males and females were both included. The authors report that a sex-based analysis found no significant differences, although the data were not shown.

Limitations noted

• No universal senescence marker. As the authors note, senescence was inferred from a combination of markers rather than identified definitively [1].
• Whole-heart lysates may mask changes in specific cell types, which could explain why the SASP findings differed from the cell-level findings.
• Sample sizes were modest (roughly 11–16 animals per group at the end of the study).
• This is a mouse study. The authors note that further investigation is needed, and findings in mice cannot be extrapolated to other species.

Why it matters for researchers

The study adds long-duration data on two very different ways of influencing senescence in a single tissue. It also illustrates a methodological point that recurs throughout senescence research: results can differ depending on whether markers are measured cell by cell or in whole-tissue samples [2]. For background on these markers, see Cellular senescence explained. For more on D+Q and other senolytics in the literature, see What are senolytics?

Note: dasatinib and quercetin are discussed here as part of the published literature only. Corex Vitality™ does not sell them.

References

1. Bevington RT, Johnson AL, Hockey BL, Fajardo VA, Parise G. Chronic senolytic treatment and/or aerobic exercise reduce senescence and improve myocardial function during aging in the heart. Aging Cell. 2026;25(10):e70759. PubMed: https://pubmed.ncbi.nlm.nih.gov/42841582/ · DOI: https://doi.org/10.1111/acel.70759
2. Gorgoulis V, Adams PD, Alimonti A, et al. Cellular senescence: defining a path forward. Cell. 2019;179(4):813-827. PubMed: https://pubmed.ncbi.nlm.nih.gov/31675495/ · DOI: https://doi.org/10.1016/j.cell.2019.10.005

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