Evidence map›Paper›PMID 23213348›Full record

ReviewOxidative medicine and cellular longevity2012

DNA mismatch repair system: repercussions in cellular homeostasis and relationship with aging.

Juan Cristóbal Conde-Pérezprina, Miguel Ángel León-Galván, Mina Konigsberg

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Role of mismatch repair in aging.International journal of biological sciences · 2021
    Review
  9. Article
  10. Article
  11. Review
  12. Mismatch repair system in endometriotic tissue and eutopic endometrium of unaffected women.International journal of clinical and experimental pathology · 2015
    Article
  13. Article
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 at 1 institution in 1 country.

Juan Cristóbal Conde-PérezprinaUniversidad Autónoma Metropolitana Unidad Iztapalapa, 186 Avenida San Rafael Atlixco, 09340 Mexico City, DF, Mexico.
Miguel Ángel León-Galván
Mina Konigsberg
Universidad Autónoma Metropolitana · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanisms that concern DNA repair have been studied in the last years due to their consequences in cellular homeostasis. The diverse and damaging stimuli that affect DNA integrity, such as changes in the genetic sequence and modifications in gene expression, can disrupt the steady state of the cell and have serious repercussions to pathways that regulate apoptosis, senescence, and cancer. These altered pathways not only modify cellular and organism longevity, but quality of life ("health-span"). The DNA mismatch repair system (MMR) is highly conserved between species; its role is paramount in the preservation of DNA integrity, placing it as a necessary focal point in the study of pathways that prolong lifespan, aging, and disease. Here, we review different insights concerning the malfunction or absence of the DNA-MMR and its impact on cellular homeostasis. In particular, we will focus on DNA-MMR mechanisms regulated by known repair proteins MSH2, MSH6, PMS2, and MHL1, among others.

Indexed as

DNA Mismatch RepairHomeostasisAgingAnimalsCell Cycle CheckpointsDNA Repair EnzymesHumansTelomere ShorteningDNA Repair Enzymes

Identifiers

PMID23213348
PMCPMC3504481
OpenAlexW2111700006

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.