Evidence map›Paper›PMID 34562508›Full record

ArticleMechanisms of ageing and development2021

Analysis of representative mutants for key DNA repair pathways on healthspan in Caenorhabditis elegans.

Lucile Marchal, Shruthi Hamsanathan, Roshan Karthikappallil, Suhao Han, Himaly Shinglot, Aditi U Gurkar

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Mechanisms of ageing and development, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 55% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Article
  3. 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

6 authors at 3 institutions in 1 country.

Lucile MarchalAging Institute of UPMC and the University of Pittsburgh School of Medicine, 100 Technology Dr, Pittsburgh, PA, 15219, USA.
Shruthi HamsanathanAging Institute of UPMC and the University of Pittsburgh School of Medicine, 100 Technology Dr, Pittsburgh, PA, 15219, USA.
Roshan KarthikappallilAging Institute of UPMC and the University of Pittsburgh School of Medicine, 100 Technology Dr, Pittsburgh, PA, 15219, USA; Medical Sciences Division, University of Oxford, Oxford, UK.
Suhao HanAging Institute of UPMC and the University of Pittsburgh School of Medicine, 100 Technology Dr, Pittsburgh, PA, 15219, USA.
Himaly ShinglotAging Institute of UPMC and the University of Pittsburgh School of Medicine, 100 Technology Dr, Pittsburgh, PA, 15219, USA.
Aditi U GurkarAging Institute of UPMC and the University of Pittsburgh School of Medicine, 100 Technology Dr, Pittsburgh, PA, 15219, USA; Division of Geriatric Medicine, Department of Medicine, University of Pittsburgh School of Medicine, 3471 Fifth Avenue, Kaufmann Medical Building Suite 500, Pittsburgh, PA, 15213, USA; Geriatric Research, Education and Clinical Centre, Veterans Affairs Pittsburgh Healthcare System, Pittsburgh, PA, 15240, USA. Electronic address: agurkar1@pitt.edu.
University of Pittsburgh · USUniversity of Pittsburgh Medical Center · USVA Pittsburgh Healthcare System · US

Funding

Modulators of DNA damage associated nucleo-mitochondrial communication in agingR00AG049126 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GURKAR, ADITI U · 2017 to 2019
$835k
NIA NIH HHS R00 AG049126
6 · The paper itself

Abstract

Although the link between DNA damage and aging is well accepted, the role of different DNA repair proteins on functional/physiological aging is not well-defined. Here, using Caenorhabditis elegans, we systematically examined the effect of three DNA repair genes involved in key genome stability pathways. We assayed multiple health proxies including molecular, functional and resilience measures to define healthspan. Loss of XPF-1/ERCC-1, a protein involved in nucleotide excision repair (NER), homologous recombination (HR) and interstrand crosslink (ICL) repair, showed the highest impairment of functional and stress resilience measures along with a shortened lifespan. brc-1 mutants, with a well-defined role in HR and ICL are short-lived and highly sensitive to acute stressors, specifically oxidative stress. In contrast, ICL mutant, fcd-2 did not impact lifespan or most healthspan measures. Our efforts also uncover that DNA repair mutants show high sensitivity to oxidative stress with age, suggesting that this measure could act as a primary proxy for healthspan. Together, these data suggest that impairment of multiple DNA repair genes can drive functional/physiological aging. Further studies to examine specific DNA repair genes in a tissue specific manner will help dissect the importance and mechanistic role of these repair systems in biological aging.

Indexed as

AgingAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsDNA DamageDNA HelicasesDNA RepairGenomic InstabilityHumansLongevityMutationOxidative StressRecombinational DNA RepairBRC-1 protein, C elegansCaenorhabditis elegans ProteinsDNA HelicasesXPF-1 protein, C elegansAgingBiological agingDNA repairHealthspanStress responses

Identifiers

PMID34562508
PMCPMC8627479
OpenAlexW3201487241

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.