Evidence map›Paper›PMID 42286666›Full record

ReviewCell & bioscience2026

Molecular mechanisms and recent advances in cellular senescence.

Ashaq Hussain, Marc Tatar, Rujun Gong

Abstract readReview
In one paragraph

Review in Cell & bioscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

3 authors.

Ashaq HussainUniversity of Toledo Medical Center, Health Science Campus, University of Toledo, Toledo, OH, USA.
Marc TatarEcology and Evolutionary Biology, Division of Biology and Medicine at Brown University, Providence, RI, USA.
Rujun GongUniversity of Toledo Medical Center, Health Science Campus, University of Toledo, Toledo, OH, USA. Rujun.Gong@UToledo.edu.

Funding

Age remodels kidney-adrenal-heart interorgan communicationU01AG086161 · NIA · BROWN UNIVERSITY · PI Rujun Gong, MARC TATAR · 2024 to 2026
$1.9M
Role of GSK3beta in diabetic kidney diseaseR01DK133203 · NIDDK · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI Rujun Gong · 2022 to 2026
$1.7M
National institute of health, USA DK133203 and AG086161NIA NIH HHS U01 AG086161NIDDK NIH HHS R01 DK133203
6 · The paper itself

Abstract

Senescence is an adaptive cellular mechanism initiated in response to diversified intrinsic and extrinsic stress stimuli, that lead to altered cellular and pathophysiological state. In this article we will review the comprehensive role of variable factors like oxidative stress, telomere attrition and oncogene activation in the initiation of senescence. Cells have a robust Redox system in place to counteract the effects of ROS/RNS mediated cell organelles and macromolecular damage to prevent senescence. The morphological, physiological and metabolic changes associated with progression of senescence and their molecular regulation at transcriptional and posttranscriptional levels has also been highlighted. The signaling pathways like p53/p21 and p16/pRB governing the senescence associated proliferative arrest and other complex cellular mechanisms that modulate the development and regulation of senescence associated secretory phenotype has been discussed in detail.

Indexed as

Cell cycle arrestDNA damageInflammationLysosomeROSSASPSenescenceTranscription

Identifiers

PMID42286666
PMCPMC13488074

What OpenQuestion 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 OpenQuestion graph.