ArticleCardiovascular research2011
Rad GTPase inhibits cardiac fibrosis through connective tissue growth factor.
Article in Cardiovascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 67 citations in OpenAlex.
- Trial
- Cellular and molecular cross-talk in atrial fibrillation: The role of non-cardiomyocytes in creating an arrhythmogenic substrate.The Journal of physiology · 2026Review
- RRAD-reduction reveals efficacy of targeting L-type calcium channel regulation for treatment of heart failure.Cardiovascular research · 2025Article
- CD11b Blockade Ameliorates Myocardial Ischemia/Reperfusion Injury by Reducing Neutrophil and Monocyte Infiltration.Journal of the American Heart Association · 2025Article
- Basic biology and roles of CEBPD in cardiovascular disease.Cell death discovery · 2025Review
- CircMYH9/miR-133a-3p/CXCR4 axis: a novel regulatory network in sperm fertilization and embryo development.Molecular biomedicine · 2024Article
- DoxoDB: A Database for the Expression Analysis of Doxorubicin-Induced lncRNA Genes.Non-coding RNA · 2023Article
- Exosomal microRNA-342-5p secreted from adipose-derived mesenchymal stem cells mitigates acute kidney injury in sepsis mice by inhibiting TLR9.Biological procedures online · 2023Article
- Genetic Disruption of Guanylyl Cyclase/Natriuretic Peptide Receptor-A Triggers Differential Cardiac Fibrosis and Disorders in Male and Female Mutant Mice: Role of TGF-β1/SMAD Signaling Pathway.International journal of molecular sciences · 2022Article
- CCAAT/Enhancer-Binding Proteins in Fibrosis: Complex Roles Beyond Conventional Understanding.Research (Washington, D.C.) · 2022Review
- Endothelial ERG alleviates cardiac fibrosis via blocking endothelin-1-dependent paracrine mechanism.Cell biology and toxicology · 2021Article
- High-Throughput Screening for CEBPD-Modulating Compounds in THP-1-Derived Reporter Macrophages Identifies Anti-Inflammatory HDAC and BET Inhibitors.International journal of molecular sciences · 2021Article
- RAD-Deficient Human Cardiomyocytes Develop Hypertrophic Cardiomyopathy Phenotypes Due to Calcium Dysregulation.Frontiers in cell and developmental biology · 2020Article
- Targeting Rho-associated coiled-coil forming protein kinase (ROCK) in cardiovascular fibrosis and stiffening.Expert opinion on therapeutic targets · 2020Review
- Ras associated with diabetes may play a role in fracture nonunion development in rats.BMC musculoskeletal disorders · 2019Article
- Myocardial-restricted ablation of the GTPase RAD results in a pro-adaptive heart response in mice.The Journal of biological chemistry · 2019Article
- Rad GTPase deletion attenuates post-ischemic cardiac dysfunction and remodeling.JACC. Basic to translational science · 2018Article
- Cardiac fibrosis: new insights into the pathogenesis.International journal of biological sciences · 2018 · on this mapReview
- Rad GTPase is essential for the regulation of bone density and bone marrow adipose tissue in mice.Bone · 2017Article
- Chromatin-remodelling factor Brg1 regulates myocardial proliferation and regeneration in zebrafish.Nature communications · 2016Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
aimsOur previous studies documented that Rad (Ras associated with diabetes), a member of the RGK (Rad, Gem, and Kir) family of Ras-related small G protein, is significantly decreased in human failing hearts and plays an important role in attenuating cardiac hypertrophy. The goal of this study is to identify the effect of Rad on cardiac fibrosis and the underlying mechanisms. METHODS AND
resultsRad knockout (KO) mice showed more severe cardiac fibrosis compared with wild-type littermate controls as detected by Sirius Red staining. Western blot analyses demonstrated that the expression of connective tissue growth factor (CTGF), a key mediator of fibrosis, increased dramatically in Rad KO mice. Overexpression of Rad in cultured neonatal cardiomyocytes suppressed both basal and transforming growth factor-β1-induced CTGF expression. Elevated CTGF expression was observed in cardiomyocytes when Rad was reduced by RNA interference. Moreover, cardiac fibroblasts produced greater extracellular matrix (ECM) when stimulated with conditioned medium from Rad-knockdown cardiomyocytes. ECM production was completely abolished by adding a CTGF-neutralizing antibody into the medium. CCAAT/enhancer-binding protein δ (C/EBP-δ) was demonstrated to activate CTGF in cardiomyocytes. Chromatin immunoprecipitation assay and co-immunoprecipitation further demonstrated that Rad inhibited the binding of C/EBP-δ to the CTGF promoter via direct interaction with C/EBP-δ.
conclusionOur data reveal that Rad deficiency can lead to cardiac fibrosis. Rad inhibits CTGF expression through binding with C/EBP-δ, thus regulating ECM production in the heart. This study suggests a potential link between decreased Rad levels and increased cardiac fibrosis in human failing hearts.
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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.