ReviewEuropean cardiology2026
The Biological Mechanisms of Frailty: Focusing on Cellular Senescence.
Review in European cardiology, 2026. 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.
- Enhancing Cardiovascular Care in Frailty: Priorities for Future Research.European cardiology · 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
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Frailty is a multifaceted clinical syndrome characterised by diminished physiological reserve and heightened vulnerability to stressors, predominantly affecting older adults. Increasing evidence implicates cellular senescence (a largely irreversible state of cell-cycle arrest accompanied by the senescence-associated secretory phenotype) as a central mechanistic driver in the pathogenesis of frailty. The aim of this review is to provide an overview of cellular senescence and examine how the accumulation of senescent cells across multiple organ systems disrupts tissue homeostasis, thereby promoting systemic inflammation and functional decline. Within this context, the role of circulating senescence-associated secretory phenotype factors as both drivers and potential biomarkers of frailty is explored. Furthermore, this review discusses the potential of emerging interventions targeting the senescent cell burden (senolytic and senomorphic agents) and non-pharmacological approaches to mitigate frailty-associated functional decline. Finally, the clinical implications of linking cellular senescence to frailty are outlined, and key priorities for future research aimed at improving risk stratification and therapeutic intervention are highlighted.
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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.