Evidence map›Paper›PMID 22337807›Full record

ArticleAging2012

Mitochondrial dysfunction and cell senescence--skin deep into mammalian aging.

Joao F Passos, Thomas von Zglinicki

Open access · hybridAbstract readComment
In one paragraph

Article in Aging, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 17% of its field
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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Mechanisms and Regulation of Cellular Senescence.International journal of molecular sciences · 2021
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Joao F PassosInstitute for Ageing and Health, Newcastle University, Newcastle upon Tyne, NE4 5PL, UK.
Thomas von Zglinicki
Newcastle University · GB

Funding

Biotechnology and Biological Sciences Research Council BB/H022384/1Medical Research Council G0900686
6 · The paper itself

Abstract

Thus, we are again left with a chicken-and egg situation: Is disrupted Ca2+ signalling, reduced mTOR activity and increased autophagy found in SOD2-/- cells because there are more senescent cells in the examined population? Or is any of these factors the culprit that triggers senescence in the first place? While the answer to these questions still eludes us, the study from Campisi and colleagues highlights the importance of mitochondrial dysfunction and cellular senescence in vivo and its impact on the aging process.

Identifiers

PMID22337807
PMCPMC3314168
OpenAlexW1576167641

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.