Evidence map›Paper›PMID 39341687›Full record

ReviewTrends in genetics : TIG2024

Genetic origins, regulators, and biomarkers of cellular senescence.

Grasiela Torres, Ivan A Salladay-Perez, Anika Dhingra, Anthony J Covarrubias

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Trends in genetics : TIG, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. p21Nature aging · 2026
    Article
  6. Article
  7. Review
  8. Aging, cellular senescence and Parkinson's disease.Journal of Parkinson's disease · 2025
    Review
  9. Review
  10. Article
  11. Article
  12. Cellular Senescence in Skin Wound Repair: Dual Roles and Senotherapeutic Interventions.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society
    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

4 authors.

Grasiela TorresDepartment of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA, USA; Molecular Biology Interdepartmental Doctoral Program, University of California, Los Angeles, Los Angeles, CA, USA; Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA, USA.
Ivan A Salladay-PerezDepartment of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA, USA; Molecular Biology Interdepartmental Doctoral Program, University of California, Los Angeles, Los Angeles, CA, USA; Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA, USA.
Anika DhingraDepartment of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA, USA.
Anthony J CovarrubiasDepartment of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA, USA; Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA, USA. Electronic address: AJCovarrubias@mednet.ucla.edu.

Funding

Transgenic & Knock-out MouseP30DK063491 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MILES Frome WILKINSON · 2003 to 2026
$40.4M
MULTIDISCIPLINARY TRAINING IN MICROBIAL PATHOGENESIST32AI007323 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Peter John Bradley · 1988 to 2026
$8.6M
Research Training in Cell and Molecular BiologyT32GM145388 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Jorge Torres · 2022 to 2026
$5.2M
UCLA LIFT-UP (Leveraging Institutional support For Talented, Upcoming Physicians and/or Scientists)U24DK132746 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI OBIDIUGWU KENRIK DURU, CAROL M MANGIONE · 2022 to 2026
$3.2M
NIAID NIH HHS T32 AI007323NIDDK NIH HHS P30 DK063491NIDDK NIH HHS U24 DK132746NIGMS NIH HHS T32 GM145388
6 · The paper itself

Abstract

This review comprehensively examines the molecular biology and genetic origins of cellular senescence. We focus on various cellular stressors and pathways leading to senescence, including recent advances in the understanding of the genetic influences driving senescence, such as telomere attrition, chemotherapy-induced DNA damage, pathogens, oncogene activation, and cellular and metabolic stress. This review also highlights the complex interplay of various signaling and metabolic pathways involved in cellular senescence and provides insights into potential therapeutic targets for aging-related diseases. Furthermore, this review outlines future research directions to deepen our understanding of senescence biology and develop effective interventions targeting senescent cells (SnCs).

Indexed as

BiomarkersCellular SenescenceDNA DamageAgingAnimalsHumansSignal TransductionTelomereBiomarkersagingcellular senescenceSASP

Identifiers

PMID39341687
PMCPMC11717094

What OpenQuestion holds

Textmetadata
LicenceTDM
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.