Evidence map›Paper›PMID 27288435›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2016

Ataxia telangiectasia-mutated kinase deficiency exacerbates left ventricular dysfunction and remodeling late after myocardial infarction.

Laura L Daniel, Stephanie L C Scofield, Patsy Thrasher, Suman Dalal, Christopher R Daniels, Cerrone R Foster, Mahipal Singh, Krishna Singh

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

Article in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
3.5field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 22 citations in OpenAlex.

  1. Guidelines for in vivo mouse models of myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2021
    Guideline
  2. Guidelines for measuring cardiac physiology in mice.American journal of physiology. Heart and circulatory physiology · 2018
    Guideline
  3. Review
  4. Article
  5. Low-power infrared laser modulates mRNA levels from genes of base excision repair and genomic stabilization in heart tissue from an experimental model of acute lung injury.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2022
    Article
  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. Article
  13. Article
  14. Article
  15. Ataxia telangiectasia mutated kinase is an autophagic balancer at the onset of heart failure.American journal of physiology. Heart and circulatory physiology · 2018
    Article
  16. Ataxia-Telangiectasia Mutated Kinase: Role in Myocardial Remodeling.Journal of rare diseases research & treatment · 2017
    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

8 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, Tennessee;
Stephanie L C ScofieldDepartment of Biomedical Sciences, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee;
Patsy ThrasherDepartment of Biomedical Sciences, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee;
Suman DalalDepartment of Biomedical Sciences, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee;
Christopher R DanielsDepartment of Biomedical Sciences, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee;
Cerrone R FosterDepartment of Biomedical Sciences, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee; Department of Biological Sciences, East Tennessee State University, Johnson City, Tennessee;
Mahipal SinghDepartment of Biomedical Sciences, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee;
Krishna SinghDepartment of Biomedical Sciences, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee; Center for Inflammation, Infectious Disease and Immunity, East Tennessee State University, Johnson City, Tennessee; James H. Quillen Veterans Affairs Medical Center, Mountain Home, Johnson City, Tennessee singhk@etsu.edu.
East Tennessee State University · US

Funding

Role of ATM in Myocardial Remodeling following Myocardial InfarctionR15HL129140 · NHLBI · EAST TENNESSEE STATE UNIVERSITY · PI SINGH, MAHIPAL · 2015 to 2015
$423k
ER stress: role in myocyte apoptosis and myocardial remodelingI01BX000640 · VA · JAMES H QUILLEN VA MEDICAL CENTER · PI SINGH, KRISHNA · 2011 to 2013
–
Osteopontin: role in myocyte apoptosis and myocardial functionI01BX002332 · VA · JAMES H QUILLEN VA MEDICAL CENTER · PI SINGH, KRISHNA · 2014 to 2017
–
BLRD VA I01 BX000640BLRD VA I01 BX002332NHLBI NIH HHS R15 HL129140
6 · The paper itself

Abstract

Ataxia telangiectasia-mutated kinase (ATM), a cell cycle checkpoint protein, is activated in response to DNA damage and oxidative stress. We have previously shown that ATM deficiency is associated with increased apoptosis and fibrosis and attenuation of cardiac dysfunction early (1-7 days) following myocardial infarction (MI). Here, we tested the hypothesis that enhanced fibrosis and apoptosis, as observed early post-MI during ATM deficiency, exacerbate cardiac dysfunction and remodeling in ATM-deficient mice late post-MI. MIs were induced in wild-type (WT) and ATM heterozygous knockout (hKO) mice by ligation of the left anterior descending artery. Left ventricular (LV) structural and functional parameters were assessed by echocardiography 14 and 28 days post-MI, whereas biochemical parameters were measured 28 days post-MI. hKO-MI mice exhibited exacerbated LV dysfunction as observed by increased LV end-systolic volume and decreased percent fractional shortening and ejection fraction. Infarct size and thickness were not different between the two genotypes. Myocyte cross-sectional area was greater in hKO-MI group. The hKO-MI group exhibited increased fibrosis in the noninfarct and higher expression of α-smooth muscle actin (myofibroblast marker) in the infarct region. Apoptosis and activation of GSK-3β (proapoptotic kinase) were significantly lower in the infarct region of hKO-MI group. Matrix metalloproteinase 2 (MMP-2) expression was not different between the two genotypes. However, MMP-9 expression was significantly lower in the noninfarct region of hKO-MI group. Thus ATM deficiency exacerbates cardiac remodeling late post-MI with effects on cardiac function, fibrosis, apoptosis, and myocyte hypertrophy.

Indexed as

ActinsAnimalsApoptosisAtaxia Telangiectasia Mutated ProteinsBlotting, WesternCell SizeCoronary VesselsEchocardiographyFemaleFibrosisGlycogen Synthase Kinase 3 betaImmunohistochemistryIn Situ Nick-End LabelingLigationMaleMatrix Metalloproteinase 2Actinsalpha-smooth muscle actin, mouseAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseGlycogen Synthase Kinase 3 betaMatrix Metalloproteinase 2Matrix Metalloproteinase 9Mmp2 protein, mouseMmp9 protein, mouseapoptosisataxia telangiectasia-mutated kinasecardiac remodelingfibrosishypertrophymyocardial infarction

Identifiers

PMID27288435
PMCPMC5005283
OpenAlexW2410531044

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.