Evidence map›Paper›PMID 39981516›Full record

ArticleiScience2025

The hypertrophic cardiomyopathy-associated A331P actin variant enhances basal contractile activity and elicits resting muscle dysfunction.

Matthew H Doran, Michael J Rynkiewicz, Evan Despond, Meera C Viswanathan, Aditi Madan, Kripa Chitre, Axel J Fenwick, Duncan Sousa, William Lehman, John F Dawson and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 2025. 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
–field-weighted citation impact
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.

  1. Article
  2. 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

11 authors.

Matthew H DoranDepartment of Pharmacology, Physiology & Biophysics, Boston University Chobanian & Avedisian School of Medicine, 72 E. Concord St, Boston, MA 02118, USA.
Michael J RynkiewiczDepartment of Pharmacology, Physiology & Biophysics, Boston University Chobanian & Avedisian School of Medicine, 72 E. Concord St, Boston, MA 02118, USA.
Evan DespondDepartment Molecular and Cellular Biology, University of Guelph, 50 Stone Road E, Guelph, ON N1G 2W1, Canada.
Meera C ViswanathanDepartment of Medicine, Division of Cardiology, Johns Hopkins University, 720 Rutland Avenue, Baltimore, MD 21205, USA.
Aditi MadanDepartment of Medicine, Division of Cardiology, Johns Hopkins University, 720 Rutland Avenue, Baltimore, MD 21205, USA.
Kripa ChitreDepartment of Medicine, Division of Cardiology, Johns Hopkins University, 720 Rutland Avenue, Baltimore, MD 21205, USA.
Axel J FenwickDepartment of Medicine, Division of Cardiology, Johns Hopkins University, 720 Rutland Avenue, Baltimore, MD 21205, USA.
Duncan SousaDepartment of Biophysics, Johns Hopkins University, 725 N. Wolfe Street, Baltimore, MD 21205, USA.
William LehmanDepartment of Pharmacology, Physiology & Biophysics, Boston University Chobanian & Avedisian School of Medicine, 72 E. Concord St, Boston, MA 02118, USA.
John F DawsonDepartment Molecular and Cellular Biology, University of Guelph, 50 Stone Road E, Guelph, ON N1G 2W1, Canada.
Anthony CammaratoDepartment of Medicine, Division of Cardiology, Johns Hopkins University, 720 Rutland Avenue, Baltimore, MD 21205, USA.

Funding

THIN FILAMENTS AND VERTEBRATE SMOOTH MUSCLE CONTRACTIONR01HL036153 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI William J Lehman · 1986 to 2026
$6.5M
PATHOGENESIS AND IN VIVO SUPPRESSION OF THIN FILAMENT-BASED CARDIOMYOPATHIESR01HL124091 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI Anthony Cammarato · 2015 to 2026
$4.3M
Thin Filaments and Muscle RegulationR37HL036153 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LEHMAN, WILLIAM J · 2008 to 2017
$4.1M
Pathogenesis and in vivo suppression of thin filament based cardiomyopathiesR56HL124091 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI CAMMARATO, ANTHONY · 2014 to 2014
$383k
NHLBI NIH HHS R01 HL036153NHLBI NIH HHS R01 HL124091NHLBI NIH HHS R37 HL036153NHLBI NIH HHS R56 HL124091
6 · The paper itself

Abstract

Previous studies aimed at defining the mechanistic basis of hypertrophic cardiomyopathy caused by A331P cardiac actin have reported conflicting results. The mutation is located along an actin surface strand, proximal to residues that interact with tropomyosin. These F-actin-tropomyosin associations are vital for proper contractile inhibition. To help resolve disease pathogenesis, we implemented a multidisciplinary approach. Transgenic

Indexed as

Biological sciencesCell biologyMolecular interactionMolecular StructureStructural biology

Identifiers

PMID39981516
PMCPMC11841076

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.