Evidence map›Paper›PMID 30346102›Full record

ReviewAging cell2019

Integrating cellular senescence with the concept of damage accumulation in aging: Relevance for clearance of senescent cells.

Mikolaj Ogrodnik, Hanna Salmonowicz, Vadim N Gladyshev

Erratum issuedAbstract readReview
In one paragraph

Review in Aging cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing 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

97 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Cellular senescence and aging: molecular mechanisms and convergent pathways.Cellular and molecular life sciences : CMLS · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Young cardiac telocyte-derived exosomes rejuvenate aging hearts in rats.Frontiers in cell and developmental biology · 2026
    Article
  13. Article
  14. Observational
  15. Review
  16. Review
  17. Article
  18. Review
  19. Quiescence Multiverse.Biomolecules · 2025
    Review
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Mikolaj OgrodnikInstitute for Cell and Molecular Biosciences, Newcastle University Institute for Ageing, Newcastle upon Tyne, UK.ORCID 0000-0003-3137-2037
Hanna SalmonowiczInstitute for Cell and Molecular Biosciences, Newcastle University Institute for Ageing, Newcastle upon Tyne, UK.ORCID 0000-0002-9444-1039
Vadim N GladyshevDivision of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.ORCID 0000-0002-0372-7016

Funding

The role of hyaluronan in longevity and cancer resistance of longest-lived rodentP01AG047200 · NIA · UNIVERSITY OF ROCHESTER · PI Andrei Seluanov · 2014 to 2026
$36.9M
Mechanisms of lifespan controlDP1AG047745 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI GLADYSHEV, VADIM N. · 2013 to 2018
$4.4M
Biotechnology and Biological Sciences Research CouncilMedical Research CouncilNIA NIH HHS DP1 AG047745NIA NIH HHS P01 AG047200NIH
6 · The paper itself

Abstract

Understanding the aging process and ways to manipulate it is of major importance for biology and medicine. Among the many aging theories advanced over the years, the concept most consistent with experimental evidence posits the buildup of numerous forms of molecular damage as a foundation of the aging process. Here, we discuss that this concept integrates well with recent findings on cellular senescence, offering a novel view on the role of senescence in aging and age-related disease. Cellular senescence has a well-established role in cellular aging, but its impact on the rate of organismal aging is less defined. One of the most prominent features of cellular senescence is its association with macromolecular damage. The relationship between cell senescence and damage concerns both damage as a molecular signal of senescence induction and accelerated accumulation of damage in senescent cells. We describe the origin, regulatory mechanisms, and relevance of various damage forms in senescent cells. This view on senescent cells as carriers and inducers of damage puts new light on senescence, considering it as a significant contributor to the rise in organismal damage. Applying these ideas, we critically examine current evidence for a role of cellular senescence in aging and age-related diseases. We also discuss the differential impact of longevity interventions on senescence burden and other types of age-related damage. Finally, we propose a model on the role of aging-related damage accumulation and the rate of aging observed upon senescent cell clearance.

Indexed as

AnimalsCell Cycle CheckpointsCellular SenescenceDNA DamageDNA RepairHumansLongevityMiceMutation AccumulationOxidative StressProteinsProteinsagingcellular senescencedeleteriomeevolutionary biologylifespanmolecular damagetheories of aging

Identifiers

PMID30346102
PMCPMC6351832

What OpenQuestion holds

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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.