Evidence map›Paper›PMID 28724653›Full record

ArticleJournal of the American Heart Association2017

Haplodeficiency of Ataxia Telangiectasia Mutated Accelerates Heart Failure After Myocardial Infarction.

Lixin Jia, Wenmei Zhang, Youcai Ma, Boya Chen, Yan Liu, Chunmei Piao, Yuan Wang, Min Yang, Tingting Liu, Junmeng Zhang and 3 more

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

Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.2field-weighted citation impact, top 18% 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

23 citing papers in PubMed, 42 citations in OpenAlex.

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  14. Metabolic regulation of endothelial senescence.Frontiers in cardiovascular medicine · 2023
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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

13 authors at 3 institutions in 1 country.

Lixin JiaBeijing Anzhen Hospital, Capital Medical University Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China.
Wenmei ZhangBeijing Anzhen Hospital, Capital Medical University Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China.
Youcai MaBeijing Anzhen Hospital, Capital Medical University Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China.
Boya ChenBeijing Anzhen Hospital, Capital Medical University Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China.
Yan LiuBeijing Anzhen Hospital, Capital Medical University Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China.
Chunmei PiaoBeijing Anzhen Hospital, Capital Medical University Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China.
Yuan WangBeijing Anzhen Hospital, Capital Medical University Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China.
Min YangBeijing Anzhen Hospital, Capital Medical University Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China.
Tingting LiuBeijing Anzhen Hospital, Capital Medical University Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China.
Junmeng ZhangBeijing Anzhen Hospital, Capital Medical University Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China.
Taotao LiBeijing Anzhen Hospital, Capital Medical University Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China.
Shaoping NieEmergency & Critical Care Center, Beijing Anzhen Hospital, Capital Medical University, Beijing, China jdu@bcm.edu spnie@126.com.
Jie DuBeijing Anzhen Hospital, Capital Medical University Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China jdu@bcm.edu spnie@126.com.
Beijing Institute of Water · CNCapital Medical University · CNBeijing Anzhen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCell senescence is involved in the process of organ damage and repair; however, the underlying molecular mechanism needs to be further explored. METHODS AND

resultsSenescence-related genes (ie, p21, p53, and ataxia telangiectasia mutated [ATM]) were shown to be elevated after myocardial infarction (MI) in both mouse and human hearts. Ten- to 12-week-old male wild-type littermates (ATM

conclusionsThe present study shows that ATM haplodeficiency decreases fibroblast senescence and vascular endothelial growth factor production and impaired angiogenesis in response to MI, leading to accelerated heart failure.

Indexed as

HaploinsufficiencyActinsAnimalsAtaxia Telangiectasia Mutated ProteinsCellular SenescenceCyclin-Dependent Kinase Inhibitor p19Disease Models, AnimalDisease ProgressionFibrosisGenetic Predisposition to DiseaseHeart FailureMaleMice, Inbred C57BLMice, KnockoutMyocardial InfarctionMyocardiumActa2 protein, mouseActinsAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseCdkn2d protein, mouseCyclin-Dependent Kinase Inhibitor p19Platelet Endothelial Cell Adhesion Molecule-1Tumor Suppressor Protein p53Vascular Endothelial Growth Factor Avascular endothelial growth factor A, mouseangiogenesisfibroblastsmyocardial infarctionsenescencevascular endothelial growth factor

Identifiers

PMID28724653
PMCPMC5586323
OpenAlexW2739366836

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.