ArticleClinical and translational medicine2017
Deletion of Cdc42 in embryonic cardiomyocytes results in right ventricle hypoplasia.
Article in Clinical and translational medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
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- The Network of Exosomes miRNA and p-MLC2 Regulatory Pathway Induced Pathological Cardiac Hypertrophy in Vasn Deficient Mice.Journal of cellular and molecular medicine · 2025Article
- In Vivo Models of Cardiovascular Disease:Biomedicines · 2025Review
- Ultrasound Phenotype, Genetic Analysis, and Pregnancy Outcomes of Fetuses With 1p36 Deletion Syndrome.Molecular genetics & genomic medicine · 2025Article
- Network assisted analysis of de novo variants using protein-protein interaction information identified 46 candidate genes for congenital heart disease.PLoS genetics · 2022Article
- Vasorin deficiency leads to cardiac hypertrophy by targeting MYL7 in young mice.Journal of cellular and molecular medicine · 2022Article
- Review
- Systems Analysis Implicates WAVE2 Complex in the Pathogenesis of Developmental Left-Sided Obstructive Heart Defects.JACC. Basic to translational science · 2020Article
- AFrontiers in pediatrics · 2019Article
- Efficient Mining of Variants From Trios for Ventricular Septal Defect Association Study.Frontiers in genetics · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundCdc42 is a member of the Rho GTPase family and functions as a molecular switch in regulating cytoskeleton remodeling and cell polarity establishment. Inactivating Cdc42 in cardiomyocytes resulted in embryonic lethality with heart developmental defects, including ventricular septum defects and thin ventricle wall syndrome.
findingsIn this study, we have generated a Cdc42 cardiomyocyte knockout mouse line by crossing Cdc42/flox mice with myosin light chain 2a (MLC2a)-Cre mice. We found that the deletion of Cdc42 in embryonic cardiomyocytes resulted in an underdeveloped right ventricle. Microarray analysis and real-time PCR data analysis displayed that the deletion of Cdc42 decreased dHand expression level. In addition, we found evaginations in the ventricle walls of Cdc42 knockout hearts.
conclusionWe concluded that Cdc42 plays an essential role in right ventricle growth.
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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 OpenQuestion graph.