Evidence map›Paper›PMID 26529187›Full record

ArticleJournal of molecular and cellular cardiology2016

Increases of desmin and α-actinin in mouse cardiac myofibrils as a response to diastolic dysfunction.

Juan-Juan Sheng, Han-Zhong Feng, Jose R Pinto, Hongguang Wei, J-P Jin

Abstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.8field-weighted citation impact, top 24% 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

26 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. The microtubule signature in cardiac disease: etiology, disease stage, and age dependency.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Can't handle the stress? Mechanobiology and disease.Trends in molecular medicine · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

5 authors at 2 institutions in 1 country.

Juan-Juan ShengDepartment of Physiology, Wayne State University School of Medicine, Detroit, MI, USA.
Han-Zhong FengDepartment of Physiology, Wayne State University School of Medicine, Detroit, MI, USA.
Jose R PintoDepartment of Biomedical Sciences, Florida State University, Tallahassee, FL, USA.
Hongguang WeiDepartment of Physiology, Wayne State University School of Medicine, Detroit, MI, USA.
J-P JinDepartment of Physiology, Wayne State University School of Medicine, Detroit, MI, USA. Electronic address: jjin@med.wayne.edu.
Wayne State University · USFlorida State University · US

Funding

Role of Troponin T Isoforms in Nemaline MyopathyR01AR048816 · NIAMS · WAYNE STATE UNIVERSITY · PI JIN, JIAN-PING · 2003 to 2014
$3.2M
Proteolytic Regulation of Troponin T & Cardiac FunctionR01HL098945 · NHLBI · WAYNE STATE UNIVERSITY · PI JIN, JIAN-PING · 2010 to 2014
$2.0M
Modulators of Cardiomyopathic DiseasesR01HL128683 · NHLBI · FLORIDA STATE UNIVERSITY · PI PINTO, JOSE RENATO · 2016 to 2020
$1.8M
The Role of Cardiomyopathic Troponin C Mutations in Skeletal and Cardiac Muscle CR00HL103840 · NHLBI · FLORIDA STATE UNIVERSITY · PI PINTO, JOSE RENATO · 2012 to 2014
$717k
The Role of Cardiomyopathic Troponin C Mutations in Skeletal and Cardiac Muscle CK99HL103840 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI PINTO, JOSE RENATO · 2010 to 2011
$188k
NHLBI NIH HHS K99 HL103840NHLBI NIH HHS R00 HL103840NHLBI NIH HHS R01 HL098945NHLBI NIH HHS R01 HL128683NIAMS NIH HHS R01 AR048816
6 · The paper itself

Abstract

Up-regulation of desmin has been reported in cardiac hypertrophy and failure but the pathophysiological cause and significance remain to be investigated. By examining genetically modified mouse models representative for diastolic or systolic heart failure, we found significantly increased levels of desmin and α-actinin in the myofibrils of hearts with impaired diastolic function but not hearts with weakened systolic function. The increased desmin and α-actinin are mainly found in myofibrils at the Z-disks. Two weeks of transverse aortic constriction (TAC) induced increases of desmin and α-actinin in mouse hearts of occult diastolic failure but not in wild type or transgenic mouse hearts with mildly lowered systolic function or with increased diastolic function. The chronic or TAC-induced increase of desmin showed no proportional increase in phosphorylation, implicating an up-regulated expression rather than a decreased protein turnover. The data demonstrate a novel early response specifically to diastolic heart failure, indicating a function of the Z-disk in the challenging clinical condition of heart failure with preserved ejection fraction (HFpEF).

Indexed as

DiastoleActininAdaptation, BiologicalAnimalsBiomarkersDesminDisease Models, AnimalEchocardiographyHeart FailureMiceMyocytes, CardiacMyofibrilsSystoleVentricular DysfunctionActininBiomarkersDesminCardiac muscle sarcomereDesminDiastolic heart failureThin filament regulatory proteinsZ-diskα-Actinin

Identifiers

PMID26529187
PMCPMC6449858
OpenAlexW1934057452

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.