Evidence map›Paper›PMID 41333012›Full record

ReviewJournal of molecular and cellular cardiology plus2025

Cardiomyocyte Rac1 signaling in hypertrophy, arrhythmia, and cardiac stress adaptation.

James P Teuber, Rachel E Scissors, Matthew J Brody

Abstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology plus, 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. 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

3 authors.

James P TeuberDepartment of Pharmacology, University of Michigan, Ann Arbor, MI, USA.
Rachel E ScissorsDepartment of Pharmacology, University of Michigan, Ann Arbor, MI, USA.
Matthew J BrodyDepartment of Pharmacology, University of Michigan, Ann Arbor, MI, USA.

Funding

Defining the cardiomyocyte microdomain signaling landscape in cardiac hypertrophyR01HL167778 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Matthew Jacob Brody · 2023 to 2026
$1.9M
NHLBI NIH HHS R01 HL167778
6 · The paper itself

Abstract

Cardiovascular disease remains the leading cause of mortality globally and is often marked by pathologic cardiac remodeling including hypertrophy and fibrosis that promote the progression to heart failure. Ras-related C3 botulinum toxin substrate 1 (Rac1) is a Rho family small GTPase that acts as a molecular switch to regulate signaling pathways that contribute to cardiac development, hypertrophy, arrhythmia, and stress adaptation. Active Rac1 promotes cardiomyocyte hypertrophy

Indexed as

ArrhythmiaASK1Cardiac hypertrophyCardiomyocytesHeart failureNOX2PAK1PalmitoylationProtein kinase ARac1

Identifiers

PMID41333012
PMCPMC12666574

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.