Evidence map›Paper›PMID 25520329›Full record

ArticleJournal of the American Heart Association2014

Deficiency of ataxia telangiectasia mutated kinase delays inflammatory response in the heart following myocardial infarction.

Laura L Daniel, Christopher R Daniels, Saghar Harirforoosh, Cerrone R Foster, Mahipal Singh, Krishna Singh

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

Article in Journal of the American Heart Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Heart failure and diabetes: role of ATM.Current opinion in pharmacology · 2020
    Review
  10. Article
  11. Considering the Role of Murine Double Minute 2 in the Cardiovascular System?Frontiers in cell and developmental biology · 2019
    Review
  12. Ataxia telangiectasia mutated kinase is an autophagic balancer at the onset of heart failure.American journal of physiology. Heart and circulatory physiology · 2018
    Article
  13. Article
  14. Article
  15. Article
  16. Ataxia-Telangiectasia Mutated Kinase: Role in Myocardial Remodeling.Journal of rare diseases research & treatment · 2017
    Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Laura L DanielDepartment of Biomedical Sciences, James H Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614
Christopher R Daniels
Saghar Harirforoosh
Cerrone R Foster
Mahipal Singh
Krishna Singh
East Tennessee State University · US

Funding

Extracellular ubiquitin: role in myocyte apoptosis and myocardial remodelingR21HL092459 · NHLBI · EAST TENNESSEE STATE UNIVERSITY · PI SINGH, KRISHNA · 2009 to 2010
$392k
Role of ATM in Cardiac Myocyte Loss and Myocardial RemodelingR21HL091405 · NHLBI · EAST TENNESSEE STATE UNIVERSITY · PI SINGH, KRISHNA · 2008 to 2009
$391k
ER stress: role in myocyte apoptosis and myocardial remodelingI01BX000640 · VA · JAMES H QUILLEN VA MEDICAL CENTER · PI SINGH, KRISHNA · 2011 to 2013
–
BLRD VA I01 BX000640NHLBI NIH HHS R21 HL091405NHLBI NIH HHS R21HL-091405NHLBI NIH HHS R21 HL092459NHLBI NIH HHS R21HL-092459
6 · The paper itself

Abstract

backgroundAtaxia‐telangiectasia results from mutations in ataxia telangiectasia mutated kinase (ATM) gene. We recently reported that ATM deficiency attenuates left ventricular (LV) dysfunction and dilatation 7 days after myocardial infarction (MI) with increased apoptosis and fibrosis. Here we investigated the role of ATM in the induction of inflammatory response, and activation of survival signaling molecules in the heart acute post‐MI. METHODS AND

resultsLV structure, function, inflammatory response, and biochemical parameters were measured in wild‐type (WT) and ATM heterozygous knockout (hKO) mice 1 and 3 days post‐MI. ATM deficiency had no effect on infarct size. MI‐induced decline in heart function, as measured by changes in percent fractional shortening, ejection fraction and LV end systolic and diastolic volumes, was lower in hKO‐MI versus WT‐MI (n=10 to 12). The number of neutrophils and macrophages was significantly lower in the infarct LV region of hKO versus WT 1 day post‐MI. Fibrosis and expression of α‐smooth muscle actin (myofibroblast marker) were higher in hKO‐MI, while active TGF‐β1 levels were higher in the WT‐MI 3 days post‐MI. Myocyte cross‐sectional area was higher in hKO‐sham with no difference between the two MI groups. MMP‐9 protein levels were similarly increased in the infarct LV region of both MI groups. Apoptosis was significantly higher in the infarct LV region of hKO at both time points. Akt activation was lower, while Bax expression was higher in hKO‐MI infarct.

conclusionATM deficiency results in decreased dilative remodeling and delays inflammatory response acute post‐MI. However, it associates with increased fibrosis and apoptosis.

Indexed as

ActinsAnimalsApoptosisAtaxia Telangiectasia Mutated ProteinsDisease Models, AnimalFemaleFibrosisHeterozygoteInflammation MediatorsMacrophagesMaleMatrix Metalloproteinase 9Mice, KnockoutMyocardial ContractionMyocardial InfarctionMyocarditisActinsalpha-smooth muscle actin, mouseAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseInflammation MediatorsMatrix Metalloproteinase 9Mmp9 protein, mouseTgfb1 protein, mouseTransforming Growth Factor beta1

Identifiers

PMID25520329
PMCPMC4338722
OpenAlexW2163450876

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.