Evidence map›Paper›PMID 34262025›Full record

ArticleCell death & disease2021

ATF5, a putative therapeutic target for the mitochondrial DNA 3243A > G mutation-related disease.

Xinpei Gao, Zhixin Jiang, Xinfeng Yan, Jiping Liu, Fengwen Li, Peng Liu, Jialu Li, Yuehua Wei, Yi Eve Sun, Yinan Zhang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. AMPK Suppression Due to Obesity Drives Oocyte mtDNA Heteroplasmy via ATF5-POLG Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  7. Article
  8. Review
  9. Article
  10. How does density of the inner mitochondrial membrane influence mitochondrial performance?American journal of physiology. Regulatory, integrative and comparative physiology · 2023
    Review
  11. Review
  12. Review
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

11 authors at 4 institutions in 1 country.

Xinpei Gao *Shanghai Institute of Stem Cell Research and Clinical Translation, Shanghai East Hospital, Tongji University, School of Medicine, Shanghai, China.
Zhixin Jiang *Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai Key Laboratory of Diabetes, Department of Endocrinology and Metabolism, Shanghai, China.
Xinfeng YanShanghai East Hospital, Tongji University School of Medicine, Department of Endocrinology, Shanghai, China.
Jiping LiuShanghai Institute of Stem Cell Research and Clinical Translation, Shanghai East Hospital, Tongji University, School of Medicine, Shanghai, China.
Fengwen LiShanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai Key Laboratory of Diabetes, Department of Endocrinology and Metabolism, Shanghai, China.
Peng LiuShanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai Key Laboratory of Diabetes, Department of Endocrinology and Metabolism, Shanghai, China.
Jialu LiShanghai Institute of Stem Cell Research and Clinical Translation, Shanghai East Hospital, Tongji University, School of Medicine, Shanghai, China.
Yuehua WeiDepartment of Oncology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Yi Eve SunShanghai Institute of Stem Cell Research and Clinical Translation, Shanghai East Hospital, Tongji University, School of Medicine, Shanghai, China. yi.eve.sun@gmail.com.
Yinan ZhangShanghai Jiao Tong University Affiliated Sixth People's Hospital, The Metabolic Disease Biobank, Shanghai, China. zhyn@sjtu.edu.cn.
Congrong WangDepartment of Endocrinology & Metabolism, Shanghai Fourth People's Hospital, School of Medicine, Tongji University, Shanghai, China. crwang@tongji.edu.cn.
Shanghai East Hospital · CNShanghai Jiao Tong University · CNShanghai Sixth People's Hospital · CNTongji University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81770883National Natural Science Foundation of China (National Science Foundation of China) 82070913
6 · The paper itself

Abstract

The mitochondrial DNA m.3243A > G mutation is well-known to cause a variety of clinical phenotypes, including diabetes, deafness, and osteoporosis. Here, we report isolation and expansion of urine-derived stem cells (USCs) from patients carrying the m.3243A > G mutation, which demonstrate bimodal heteroplasmy. USCs with high levels of m.3243A > G mutation displayed abnormal mitochondrial morphology and function, as well as elevated ATF5-dependent mitochondrial unfolded protein response (UPR

Indexed as

MutationActivating Transcription FactorsAdultCase-Control StudiesCells, CulturedCell SeparationDNA, MitochondrialDNA Mutational AnalysisFemaleGenetic Predisposition to DiseaseGlycogen Synthase Kinase 3 betaHeteroplasmyHumansMaleMitochondriaMitochondrial DiseasesActivating Transcription FactorsATF5 protein, humanDNA, MitochondrialGlycogen Synthase Kinase 3 betaGSK3B protein, humanWNT7B protein, humanWnt Proteins

Identifiers

PMID34262025
PMCPMC8280182
OpenAlexW3179193651

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.