Evidence map›Paper›PMID 38527667›Full record

ArticleJournal of molecular and cellular cardiology2024

Reduced cardiac antioxidant defenses mediate increased susceptibility to workload-induced myocardial injury in males with genetic cardiomyopathy.

Tatyana A Vetter, Preethy Parthiban, Jackie A Stevens, Xavier S Revelo, Mark J Kohr, DeWayne Townsend

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

Article in Journal of molecular and cellular cardiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

6 authors at 4 institutions in 1 country.

Tatyana A VetterNationwide Children's Hospital, Columbus, OH, United States of America.
Preethy ParthibanDepartment of Integrative Biology and Physiology, University of Minnesota Medical School, Minneapolis, MN, United States of America.
Jackie A StevensDepartment of Integrative Biology and Physiology, University of Minnesota Medical School, Minneapolis, MN, United States of America.
Xavier S ReveloDepartment of Integrative Biology and Physiology, University of Minnesota Medical School, Minneapolis, MN, United States of America.
Mark J KohrDepartment of Environmental Health and Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America.
DeWayne TownsendDepartment of Integrative Biology and Physiology, University of Minnesota Medical School, Minneapolis, MN, United States of America; Greg Marzolf Jr. Muscular Dystrophy Center, University of Minnesota, Minneapolis, MN, United States of America; Lillehei Heart Institute, University of Minnesota, Minneapolis, MN, United States of America. Electronic address: town0045@umn.edu.
University of Minnesota Medical Center · USJohns Hopkins University · USNationwide Children's Hospital · USUniversity of Minnesota · US

Funding

Improving dystrophin gene therapy through understanding dystrobrevin functionR01HL114832 · NHLBI · UNIVERSITY OF MINNESOTA · PI TOWNSEND, DEWAYNE · 2013 to 2017
$1.8M
Coronary Regulation in Dystrophic CardiomyopathyK08HL102066 · NHLBI · UNIVERSITY OF MINNESOTA · PI TOWNSEND, DEWAYNE · 2010 to 2014
$641k
Female Resilience in Dystrophic CardiomyopathyF31HL139093 · NHLBI · UNIVERSITY OF MINNESOTA · PI VETTER, TATYANA A · 2017 to 2019
$71k
NHLBI NIH HHS F31 HL139093NHLBI NIH HHS K08 HL102066NHLBI NIH HHS R01 HL114832
6 · The paper itself

Abstract

Ongoing cardiomyocyte injury is a major mechanism in the progression of heart failure, particularly in dystrophic hearts. Due to the poor regenerative capacity of the adult heart, cardiomyocyte death results in the permanent loss of functional myocardium. Understanding the factors contributing to myocyte injury is essential for the development of effective heart failure therapies. As a model of persistent cardiac injury, we examined mice lacking β-sarcoglycan (β-SG), a key component of the dystrophin glycoprotein complex (DGC). The loss of the sarcoglycan complex markedly compromises sarcolemmal integrity in this β-SG

Indexed as

AntioxidantsCardiomyopathiesMyocardiumOxidative StressSarcoglycansAnimalsDisease SusceptibilityFemaleIsoproterenolMaleMiceMice, KnockoutMyocytes, CardiacReceptor, Angiotensin, Type 1AntioxidantsIsoproterenolReceptor, Angiotensin, Type 1SarcoglycansAngiotensin II type 1 receptorAntioxidantDystrophic cardiomyopathyMyocardial injuryS-nitrosylation

Identifiers

PMID38527667
PMCPMC11060907
OpenAlexW4393204028

What OpenQuestion holds

Textmetadata
LicenceTDM
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.