Evidence map›Paper›PMID 40134985›Full record

ReviewFrontiers in cardiovascular medicine2025

cMyBP-C in hypertrophic cardiomyopathy: gene therapy and small-molecule innovations.

Patrick T Wood, Morgan M Seffrood, Brett A Colson, Julian E Stelzer

Abstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

4 authors.

Patrick T WoodDepartment of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, OH, United States.
Morgan M SeffroodDepartment of Cellular & Molecular Medicine, University of Arizona, Tucson, AZ, United States.
Brett A ColsonDepartment of Cellular & Molecular Medicine, University of Arizona, Tucson, AZ, United States.
Julian E StelzerDepartment of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, OH, United States.

Funding

PHYSIOLOGYT32HL007249 · NHLBI · UNIVERSITY OF ARIZONA · PI Brett A Colson, JOHN P KONHILAS · 1985 to 2026
$12.5M
Computer modeling of myosin binding protein C and its effects on cardiac contractionR01HL146676 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI Kenneth S Campbell, Julian Stelzer · 2019 to 2026
$4.3M
Functional consequences of FHC mutations in cardiac MyBPCR01HL114770 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI STELZER, JULIAN · 2013 to 2023
$4.3M
Structural Dynamics of Cardiac Myosin-Binding Protein C RegulationR01HL141564 · NHLBI · UNIVERSITY OF ARIZONA · PI Brett A Colson · 2019 to 2026
$3.8M
Novel downstream effectors of protein kinase G in hypertensive diseaseR01HL153236 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI STELZER, JULIAN · 2021 to 2024
$2.5M
Skeletal Myosin-Binding Protein C Regulation and Structural DynamicsR01AR079435 · NIAMS · UNIVERSITY OF ARIZONA · PI Brett A Colson · 2022 to 2026
$2.4M
Biological Basis of Genetic cMyBP-C CardiomyopathiesR01HL173989 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI Kenneth S Campbell, Julian Stelzer · 2024 to 2026
$2.0M
Molecular Basis for cMyBP-C HCM variantsR01HL175803 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI KRISHNA CHINTHALAPUDI, Julian Stelzer · 2025 to 2026
$1.4M
Biological basis of cardiac thick filament regulationR01HL181868 · NHLBI · OHIO STATE UNIVERSITY · PI KRISHNA CHINTHALAPUDI, Julian Stelzer · 2025 to 2026
$1.4M
High resolution ultrasound for small animal imagingS10OD021635 · OD · CASE WESTERN RESERVE UNIVERSITY · PI STELZER, JULIAN · 2016 to 2016
$478k
NHLBI NIH HHS R01 HL114770NHLBI NIH HHS R01 HL141564NHLBI NIH HHS R01 HL146676NHLBI NIH HHS R01 HL153236NHLBI NIH HHS R01 HL173989NHLBI NIH HHS R01 HL175803NHLBI NIH HHS R01 HL181868NHLBI NIH HHS T32 HL007249NIAMS NIH HHS R01 AR079435NIH HHS S10 OD021635
6 · The paper itself

Abstract

Hypertrophic cardiomyopathy (HCM) is a genetic disorder in the heart caused by variants in sarcomeric proteins that disrupt myocardial function, leading to hypercontractility, hypertrophy, and fibrosis. Optimal cardiac function relies on the precise coordination of thin and thick filament proteins that control the timing, magnitude of cellular force generation and relaxation, and

Indexed as

AAV9 gene transfercMyBP-Cgene therapyhigh-throughput screeninghypertrophic cardiomyopathymyosin binding protein Csmall-moleculesmall molecule therapy

Identifiers

PMID40134985
PMCPMC11935118

What Socratic 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 Socratic graph.