ArticleJournal of cardiovascular development and disease2021
Myocardium-Specific Deletion of Rac1 Causes Ventricular Noncompaction and Outflow Tract Defects.
Article in Journal of cardiovascular development and disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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.
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.
Who cites it
13 citing papers in PubMed, 12 citations in OpenAlex.
- Rethinking Left Ventricular Noncompaction and Excessive Left Ventricular Trabeculation: Development, Genetics, and a Proposed Conceptual Framework.Journal of clinical medicine · 2026Review
- Cardiomyocyte Rac1 signaling in hypertrophy, arrhythmia, and cardiac stress adaptation.Journal of molecular and cellular cardiology plus · 2025Review
- Rac1 palmitoylation is required for cardiac stress adaptation and regulation of protein kinase A signaling.JCI insight · 2025Article
- Intrauterine phenotype, genetic analysis, and pregnancy follow-up of fetuses with the 16p12.2 microdeletion.Frontiers in genetics · 2025Article
- Thrombospondin 1 and Reelin act through Vldlr to regulate cardiac growth and repair.Basic research in cardiology · 2024Article
- Bifid cardiac apex and spongiform cardiomyopathy in fetus with small microdeletion 16p12.2 of paternal origin. Critical points in family communication on 16p12.2 microdeletion.Clinical case reports · 2023Article
- Clinical profiling of MRD48 and functional characterization of two novel pathogenic RAC1 variants.European journal of human genetics : EJHG · 2023Review
- Article
- Quantitative proteomic profiling identifies global protein network dynamics in murine embryonic heart development.Developmental cell · 2023Article
- Introduction to Special Issue "Leaders in Cardiovascular Research, Dedicated to the Memory of Professor Adriana Gittenberger-de Groot".Journal of cardiovascular development and disease · 2022Article
- Loss of Zic3 impairs planar cell polarity leading to abnormal left-right signaling, heart defects and neural tube defects.Human molecular genetics · 2021Article
- Overlap phenotypes of the left ventricular noncompaction and hypertrophic cardiomyopathy with complex arrhythmias and heart failure induced by the novel truncated DSC2 mutation.Orphanet journal of rare diseases · 2021Article
- Bifid Cardiac Apex in Noonan Syndrome: An Unusual Cardiac Morphology Associated with a RAF1 Pathogenic Variant.Journal of cardiovascular echographyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundLeft ventricular noncompaction (LVNC) is a cardiomyopathy that can lead to arrhythmias, embolic events and heart failure. Despite our current knowledge of cardiac development, the mechanisms underlying noncompaction of the ventricular myocardium are still poorly understood. The small GTPase METHODS AND
resultsThe
conclusions
Indexed as
Identifiers
What Socratic holds
Registered trials
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.