Evidence map›Paper›PMID 37159677›Full record

ArticleJournal of molecular and cellular cardiology plus2022

Low expression of the K280N

Vasco Sequeira, Lili Wang, Paul J M Wijnker, Kyungsoo Kim, Jose R Pinto, Cris Dos Remedios, Charles Redwood, Bjorn C Knollmann, Jolanda van der Velden

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

Article in Journal of molecular and cellular cardiology plus, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Review
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

9 authors at 6 institutions in 5 countries.

Vasco SequeiraAmsterdam UMC, Vrije Universiteit Amsterdam, Physiology, Amsterdam Cardiovascular Sciences, Amsterdam, the Netherlands.
Lili WangDivision of Clinical Pharmacology, Vanderbilt School of Medicine, Nashville, United States.
Paul J M WijnkerAmsterdam UMC, Vrije Universiteit Amsterdam, Physiology, Amsterdam Cardiovascular Sciences, Amsterdam, the Netherlands.
Kyungsoo KimDivision of Clinical Pharmacology, Vanderbilt School of Medicine, Nashville, United States.
Jose R PintoDepartment of Biomedical Sciences, College of Medicine, Florida State University, Tallahassee, FL, USA.
Cris Dos RemediosMuscle Research Unit, Discipline of Anatomy & Histology, Bosch Institute, The University of Sydney, Sydney, Australia.
Charles RedwoodRadcliffe Department of Medicine, University of Oxford, UK.
Bjorn C KnollmannDivision of Clinical Pharmacology, Vanderbilt School of Medicine, Nashville, United States.
Jolanda van der VeldenAmsterdam UMC, Vrije Universiteit Amsterdam, Physiology, Amsterdam Cardiovascular Sciences, Amsterdam, the Netherlands.
Vanderbilt University · USAmsterdam University Medical Centers · NLFlorida State University · USUniversity of Oxford · GBUniversity of Sydney · AUVrije Universiteit Amsterdam · NL

Funding

Toward a Mechanism-Based Approach to Treating Cardiac ArrhythmiaR35HL144980 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI KNOLLMANN, BJORN C · 2019 to 2025
$7.1M
The mechanisms of cardiac thin filament regulation in health and disease.R01HL160966 · NHLBI · OLD DOMINION UNIVERSITY · PI CHASE, P. BRYANT, GALKIN, VITOLD · 2022 to 2025
$2.3M
Modulators of Cardiomyopathic DiseasesR01HL128683 · NHLBI · FLORIDA STATE UNIVERSITY · PI PINTO, JOSE RENATO · 2016 to 2020
$1.8M
NHLBI NIH HHS R01 HL128683NHLBI NIH HHS R01 HL160966NHLBI NIH HHS R35 HL144980
6 · The paper itself

Abstract

Background: Hypertrophic cardiomyopathy (HCM) is an autosomal dominant genetic disorder with patients typically showing heterozygous inheritance of a pathogenic variant in a gene encoding a contractile protein. Here, we study the contractile effects of a rare homozygous mutation using explanted tissue and human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) to gain insight into how the balance between mutant and WT protein expression affects cardiomyocyte function. Methods: Force measurements were performed in cardiomyocytes isolated from a HCM patient carrying a homozygous troponin T mutation (cTnT-K280N) and healthy donors. To discriminate between mutation-mediated and phosphorylation-related effects on Ca Results: Myofilament Ca Conclusions: The cTnT-K280N mutation increases myofilament Ca

Indexed as

hiPSC-CMHypertrophic cardiomyopathyMyofilament Ca2+-sensitivityProtein toxic thresholdTroponin T

Identifiers

PMID37159677
PMCPMC10160007
OpenAlexW4281293330

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.