Evidence map›Paper›PMID 25666573›Full record

ArticleAge (Dordrecht, Netherlands)2015

Mitochondrial genomes and exceptional longevity in a Chinese population: the Rugao longevity study.

Lei Li, Hong-Xiang Zheng, Zuyun Liu, Zhendong Qin, Fei Chen, Degui Qian, Jun Xu, Li Jin, Xiaofeng Wang

Abstract read
In one paragraph

Article in Age (Dordrecht, Netherlands), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Genetic and epigenetic regulation of human aging and longevity.Biochimica et biophysica acta. Molecular basis of disease · 2019
    Review
  6. Genetic cartography of longevity in humans and mice: Current landscape and horizons.Biochimica et biophysica acta. Molecular basis of disease · 2018
    Review
  7. Article
  8. Article
  9. 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

9 authors.

Lei LiState Key Laboratory of Genetic Engineering and Ministry of Education Key Laboratory of Contemporary Anthropology, School of Life Sciences, Fudan University, Songhu Rd., Shanghai, 200433, China.
Hong-Xiang Zheng
Zuyun Liu
Zhendong Qin
Fei Chen
Degui Qian
Jun Xu
Li Jin
Xiaofeng Wang

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic variants of whole mitochondrial DNA (mtDNA) that predispose to exceptional longevity need to be systematically identified and appraised. Here, we conducted a case-control study with 237 exceptional longevity subjects (aged 95-107) and 444 control subjects (aged 40-69) randomly recruited from a "longevity town"-the city of Rugao in China-to investigate the effects of mtDNA variants on exceptional longevity. We sequenced the entire mtDNA genomes of the 681 subjects using a next-generation platform and employed a complete mtDNA phylogenetic analytical strategy. We identified T3394C as a candidate that counteracts longevity, and we observed a higher load of private nonsynonymous mutations in the COX1 gene predisposing to female longevity. Additionally, for the first time, we identified several variants and new subhaplogroups related to exceptional longevity. Our results provide new clues for genetic mechanisms of longevity and shed light on strategies for evaluating rare mitochondrial variants that underlie complex traits.

Indexed as

AdultAgedAged, 80 and overAsian PeopleCase-Control StudiesChinaDNA, MitochondrialFemaleGenome, MitochondrialHaplotypesHumansLongevityMaleMiddle AgedDNA, Mitochondrial

Identifiers

PMID25666573
PMCPMC4322039

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.