ArticleCell death & disease2014
Rnd3 haploinsufficient mice are predisposed to hemodynamic stress and develop apoptotic cardiomyopathy with heart failure.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 39 citations in OpenAlex.
- RND3 Enhances Cardiac Glucose Metabolism Through Inhibiting ACAT1-Dependent PDHA1 Acetylation and Protects Against Ischemia-Reperfusion Injury.Circulation · 2026Article
- Diabetes Advances Cardiomyocyte Senescence Through Interfering Rnd3 Expression and Function.Aging cell · 2025Article
- Rnd3 protects against doxorubicin-induced cardiotoxicity through inhibition of PANoptosis in a Rock1/Drp1/mitochondrial fission-dependent manner.Cell death & disease · 2025Article
- Identification of New Markers of Angiogenic Sprouting Using Transcriptomics: New Role for RND3.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Fibroblast-specific activation of Rnd3 protects against cardiac remodeling in diabetic cardiomyopathy via suppression of Notch and TGF-β signaling.Theranostics · 2022Article
- RND3 attenuates oxidative stress and vascular remodeling in spontaneously hypertensive rat via inhibiting ROCK1 signaling.Redox biology · 2021Article
- MicroRNA-145-5p inhibits hypoxia/reoxygenation-induced apoptosis in H9c2 cardiomyocytes by targeting ROCK1.Experimental and therapeutic medicine · 2021Article
- Maternal RND3/RhoE deficiency impairs placental mitochondrial function in preeclampsia by modulating the PPARγ-UCP2 cascade.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Inhibiting miR-205 Alleviates Cardiac Ischemia/Reperfusion Injury by Regulating Oxidative Stress, Mitochondrial Function, and Apoptosis.Oxidative medicine and cellular longevity · 2021Article
- Identification of Molecular Regulatory Features and Markers for Acute Type A Aortic Dissection.Computational and mathematical methods in medicine · 2021Article
- Identification of Key Pathways and Genes in Obesity Using Bioinformatics Analysis and Molecular Docking Studies.Frontiers in endocrinology · 2021Article
- Identification and characterization of a new isoform of small GTPase RhoE.Communications biology · 2020Article
- Ingenuity pathway analysis of differentially expressed genes involved in signaling pathways and molecular networks in RhoE gene‑edited cardiomyocytes.International journal of molecular medicine · 2020Article
- Targeting Rho-associated coiled-coil forming protein kinase (ROCK) in cardiovascular fibrosis and stiffening.Expert opinion on therapeutic targets · 2020Review
- RhoGTPase in Vascular Disease.Cells · 2019Review
- RhoE Fine-Tunes Inflammatory Response in Myocardial Infarction.Circulation · 2019Article
- Rho kinase signaling and cardiac physiology.Current opinion in physiology · 2018Article
- RND3 promotes Snail 1 protein degradation and inhibits glioblastoma cell migration and invasion.Oncotarget · 2016Article
- Rnd3 as a Novel Target to Ameliorate Microvascular Leakage.Journal of the American Heart Association · 2016Article
- Rnd3/RhoE Modulates Hypoxia-Inducible Factor 1α/Vascular Endothelial Growth Factor Signaling by Stabilizing Hypoxia-Inducible Factor 1α and Regulates Responsive Cardiac Angiogenesis.Hypertension (Dallas, Tex. : 1979) · 2016Article
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Authors and funding
13 authors at 6 institutions in 2 countries.
Funding
Abstract
Rho family guanosine triphosphatase (GTPase) 3 (Rnd3), a member of the small Rho GTPase family, has been suggested to regulate cell actin cytoskeleton dynamics, cell migration, and apoptosis through the Rho kinase-dependent signaling pathway. The biological function of Rnd3 in the heart is unknown. The downregulation of small GTPase Rnd3 transcripts was found in patients with end-stage heart failure. The pathological significance of Rnd3 loss in the transition to heart failure remains unexplored. To investigate the functional consequence of Rnd3 downregulation and the associated molecular mechanism, we generated Rnd3(+/-) haploinsufficient mice to mimic the downregulation of Rnd3 observed in the failing human heart. Rnd3(+/-) mice were viable; however, the mice developed heart failure after pressure overload by transverse aortic constriction (TAC). Remarkable apoptosis, increased caspase-3 activity, and elevated Rho kinase activity were detected in the Rnd3(+/-) haploinsufficient animal hearts. Pharmacological inhibition of Rho kinase by fasudil treatment partially improved Rnd3(+/-) mouse cardiac functions and attenuated myocardial apoptosis. To determine if Rho-associated coiled-coil kinase 1 (ROCK1) was responsible for Rnd3 deficiency-mediated apoptotic cardiomyopathy, we established a double-knockout mouse line, the Rnd3 haploinsufficient mice with ROCK1-null background (Rnd3(+/-/ROCK1-/-)). Again, genetic deletion of ROCK1 partially but not completely rescued Rnd3 deficiency-mediated heart failure phenotype. These data suggest that downregulation of Rnd3 correlates with cardiac loss of function as in heart failure patients. Animals with Rnd3 haploinsufficiency are predisposed to hemodynamic stress. Hyperactivation of Rho kinase activity is responsible in part for the apoptotic cardiomyopathy development. Further investigation of ROCK1-independent mechanisms in Rnd3-mediated cardiac remodeling should be the focus for future study.
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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.