Evidence map›Paper›PMID 36699942›Full record

ReviewLife medicine2022

Targeting senescent cells for a healthier longevity: the roadmap for an era of global aging.

Yu Sun, Qingfeng Li, James L Kirkland

Abstract readReview
In one paragraph

Review in Life medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing 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

63 citing papers in PubMed.

  1. Life (Basel, Switzerland) · 2026
    Review
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  19. Review
  20. Dissecting the Heterogeneity of Senescent Cells Through CITE-seq Integration.Methods in molecular biology (Clifton, N.J.) · 2025
    Article

3 more citing papers are in PubMed but not listed here.

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.

Yu SunCAS Key Laboratory of Tissue Microenvironment and Tumor, Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, Shanghai 200031, China.
Qingfeng LiDepartment of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China.
James L KirklandDepartment of Medicine, Mayo Clinic, Rochester, MN 55905, USA.

Funding

Targeting Cellular Senescence to Extend HealthspanP01AG062413 · NIA · MAYO CLINIC ROCHESTER · PI Sundeep Khosla · 2019 to 2026
$28.7M
ConProject-001UH3AG056933 · NIA · JOHNS HOPKINS UNIVERSITY · PI BANDEEN-ROCHE, KAREN J., VARADHAN, RAVI · 2019 to 2021
$7.0M
Effect of Aging on Preadipocyte DifferentiationR37AG013925 · NIA · MAYO CLINIC ROCHESTER · PI KIRKLAND, JAMES L. · 2016 to 2025
$6.6M
Translational Geroscience NetworkR33AG061456 · NIA · MAYO CLINIC ROCHESTER · PI JAMES L. KIRKLAND, STEPHEN B. KRITCHEVSKY · 2019 to 2026
$6.2M
COVID-FIS: A PHASE 2 PLACEBO-CONTROLLED PILOT STUDY IN COVID-19 OF FISETIN TO ALLEVIATE DYSFUNCTION AND EXCESSIVE INFLAMMATORY RESPONSE IN OLDER ADULTS IN NURSING HOMESR01AG072301 · NIA · MAYO CLINIC ROCHESTER · PI PIGNOLO, ROBERT JOHN · 2020 to 2024
$1.9M
Senescence cells as a source of pro-aging miR-146aR56AG061414 · NIA · UNIVERSITY OF CENTRAL FLORIDA · PI KIRKLAND, JAMES L., MASTERNAK, MICHAL MATEUSZ · 2019 to 2019
$406k
NIA NIH HHS P01 AG062413NIA NIH HHS R01 AG072301NIA NIH HHS R33 AG061456NIA NIH HHS R37 AG013925NIA NIH HHS R56 AG061414NIA NIH HHS UH3 AG056933
6 · The paper itself

Abstract

Aging is a natural but relentless process of physiological decline, leading to physical frailty, reduced ability to respond to physical stresses (resilience) and, ultimately, organismal death. Cellular senescence, a self-defensive mechanism activated in response to intrinsic stimuli and/or exogenous stress, is one of the central hallmarks of aging. Senescent cells cease to proliferate, while remaining metabolically active and secreting numerous extracellular factors, a feature known as the senescence-associated secretory phenotype. Senescence is physiologically important for embryonic development, tissue repair, and wound healing, and prevents carcinogenesis. However, chronic accumulation of persisting senescent cells contributes to a host of pathologies including age-related morbidities. By paracrine and endocrine mechanisms, senescent cells can induce inflammation locally and systemically, thereby causing tissue dysfunction, and organ degeneration. Agents including those targeting damaging components of the senescence-associated secretory phenotype or inducing apoptosis of senescent cells exhibit remarkable benefits in both preclinical models and early clinical trials for geriatric conditions. Here we summarize features of senescent cells and outline strategies holding the potential to be developed as clinical interventions. In the long run, there is an increasing demand for safe, effective, and clinically translatable senotherapeutics to address healthcare needs in current settings of global aging.

Indexed as

agingclinical trialsenescence-associated secretory phenotypesenescent cellsenotherapeutics

Identifiers

PMID36699942
PMCPMC9869767

What OpenQuestion holds

Textmetadata
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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.