Evidence map›Paper›PMID 42439909›Full record

ReviewCellular and molecular life sciences : CMLS2026

Cellular senescence and aging: molecular mechanisms and convergent pathways.

Francesca Cristiana Piritore, Michele Braggio, Arianna Minoia, Silvia Bolognin, Mattia Cominacini, Elisabetta Trabetti, Cristina Bombieri, Maria Grazia Romanelli, Luca Dalle Carbonare, Maria Teresa Valenti

Abstract readReview
PubMed Publisher
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Francesca Cristiana PiritoreDepartment of Neurosciences, Biomedicines and Movement Medicine, University of Verona, Verona, 37134, Italy.
Michele BraggioDepartment of Neurosciences, Biomedicines and Movement Medicine, University of Verona, Verona, 37134, Italy.
Arianna MinoiaDepartment of Engineering for Innovation Medicine, School of Medicine in Sports and Exercise, University of Verona and Azienda Ospedaliera Universitaria Integrata of Verona, Verona, 37134, Italy.
Silvia BologninMERLN Institute for Technology-Inspired Regenerative Medicine, Maastricht University, Maastricht, the Netherlands.
Mattia CominaciniDepartment of Engineering for Innovation Medicine, School of Medicine in Sports and Exercise, University of Verona and Azienda Ospedaliera Universitaria Integrata of Verona, Verona, 37134, Italy.
Elisabetta TrabettiDepartment of Neurosciences, Biomedicines and Movement Medicine, University of Verona, Verona, 37134, Italy.
Cristina BombieriDepartment of Neurosciences, Biomedicines and Movement Medicine, University of Verona, Verona, 37134, Italy.
Maria Grazia RomanelliDepartment of Neurosciences, Biomedicines and Movement Medicine, University of Verona, Verona, 37134, Italy.
Luca Dalle CarbonareDepartment of Engineering for Innovation Medicine, School of Medicine in Sports and Exercise, University of Verona and Azienda Ospedaliera Universitaria Integrata of Verona, Verona, 37134, Italy.
Maria Teresa ValentiDepartment of Neurosciences, Biomedicines and Movement Medicine, University of Verona, Verona, 37134, Italy. mariateresa.valenti@univr.it.ORCID http://orcid.org/0000-0003-1166-8033

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The frequent conceptual overlap between aging and cellular senescence has generated ambiguities in experimental approaches, biomarker usage, and therapeutic strategy development within aging research. Cellular senescence and aging are biologically distinct but interconnected processes, frequently misunderstood or used interchangeably within biomedical research and theoretical discussions. Thus, aging refers to the progressive decline in physiological integrity and function at the organismal level, while cellular senescence is a stable cell-cycle arrest triggered by various forms of stress, including DNA damage, telomere shortening, epigenetic dysregulation, and mitochondrial dysfunction. This review dissects the molecular underpinnings of both phenomena, highlighting their key differences, mechanistic overlaps, and roles in health and disease, with particular emphasis on how the accumulation of senescent cells actively contributes to age-related functional decline. In particular, we discuss emerging biomarkers and therapeutic strategies, such as senolytics and partial reprogramming. Furthermore, a deeper understanding of these processes may contribute to the identification of innovative interventions for age-related disorders, such as therapies targeting specific components of the senescence-associated secretory phenotype or selectively modulating senescent cell burden.

Indexed as

AgingCellular SenescenceAnimalsDNA DamageEpigenesis, GeneticHumansMitochondriaSenescence-Associated Secretory PhenotypeSignal TransductionEpigenetic clocksGeroscienceInflammagingSenescence-associated secretory phenotypeSenolytics

Identifiers

PMID42439909

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.