ReviewJournal of translational medicine2025
Unleashing endogenous regeneration by senolytics.
Review in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Harnessing the novel safeguarding role of Selenoprotein T in age-related myocardial left and right decline through the ferroptosis-mitochondrial axis.Journal of translational medicine · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Regenerative medicine holds significant promise for the treatment of chronic diseases by harnessing the body’s innate capacity to repair and restore physiological function. However, regenerative activity declines markedly with age, a phenomenon traditionally attributed to depletion/exhaustion of progenitor cell pools. We propose an alternative, complementary mechanism: that age-associated accumulation of senescent cells contributes to impaired regeneration through the secretion of “anti-regenerative” factors. Senolytic therapies, which selectively eliminate senescent cells, may therefore exert therapeutic effects in part by de-repressing endogenous regenerative pathways. If senolytics restore progenitor cell function, their use in combination with interventions known to stimulate endogenous progenitor activity, yet not fully optimized for clinical translation, may provide a powerful strategy to enhance tissue repair. In this review, we examine current research on cellular senescence and the therapeutic potential of senolytics across diverse chronic disease contexts. We summarize the presence and role of endogenous regenerative cells in multiple organ systems and highlight mechanisms by which senescent cell-derived secretory factors inhibit regeneration. Finally, we propose potential applications in which senolytic therapy could be leveraged to augment both homeostatic regeneration and regeneration stimulated by therapeutic interventions.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.