ArticleJournal of molecular medicine (Berlin, Germany)2017
The Rho kinase inhibitor, fasudil, ameliorates diabetes-induced cardiac dysfunction by improving calcium clearance and actin remodeling.
Article in Journal of molecular medicine (Berlin, Germany), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- Rnd3 protects against doxorubicin-induced cardiotoxicity through inhibition of PANoptosis in a Rock1/Drp1/mitochondrial fission-dependent manner.Cell death & disease · 2025Article
- Leiomodin 2 neonatal dilated cardiomyopathy mutation results in altered actin gene signatures and cardiomyocyte dysfunction.NPJ Regenerative medicine · 2024Article
- Untangling the role of RhoA in the heart: protective effect and mechanism.Cell death & disease · 2024Review
- Shared signaling pathways and comprehensive therapeutic approaches among diabetes complications.Frontiers in medicine · 2024Review
- Article
- Speckle-tracking echocardiography provides sensitive measurements of subtle early alterations associated with cardiac dysfunction in T2DM rats.BMC cardiovascular disorders · 2023Article
- Actin-Binding Proteins in Cardiac Hypertrophy.Cells · 2022Review
- Bamboo Shoot andCurrent issues in molecular biology · 2022Article
- Signaling Pathways Related to Oxidative Stress in Diabetic Cardiomyopathy.Frontiers in endocrinology · 2022Review
- Review
- Rho kinase cascade activation in circulating leukocytes in patients with diabetes mellitus type 2.Cardiovascular diabetology · 2020Observational
- Notch3 Modulates Cardiac Fibroblast Proliferation, Apoptosis, and Fibroblast to Myofibroblast Transition via Negative Regulation of the RhoA/ROCK/Hif1α Axis.Frontiers in physiology · 2020Article
- Attenuation of Diabetic Nephropathy in Diabetic Mice by Fasudil through Regulation of Macrophage Polarization.Journal of diabetes research · 2020Article
- Identification of Novel Therapeutic Targets for Pulmonary Arterial Hypertension.International journal of molecular sciences · 2018Review
- Actin-associated proteins and cardiomyopathy-the 'unknown' beyond troponin and tropomyosin.Biophysical reviews · 2018Review
- Regulation of autophagy by tea polyphenols in diabetic cardiomyopathy.Journal of Zhejiang University. Science. B · 2018Article
- Progressive Decrease in Coronary Vascular Function Associated With Type 2 Diabetic Heart Disease.Frontiers in physiology · 2018Article
- Prenatal Hypoxia Induced Dysfunction in Cerebral Arteries of Offspring Rats.Journal of the American Heart Association · 2017Article
- Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes.Journal of visualized experiments : JoVE · 2017Article
- Downregulation of Profilin-1 Expression Attenuates Cardiomyocytes Hypertrophy and Apoptosis Induced by Advanced Glycation End Products in H9c2 Cells.BioMed research international · 2017Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous study showed inhibition of RhoA and Rho kinase (ROCK) activity with fasudil could alleviate diabetes-induced cardiac dysfunction partially due to improvement of myocardial fibrosis. However, the effect of fasudil on intracellular calcium cycling and actin remodeling, both of which are important to regulate excitation-contract coupling, is still not fully elucidated. In this study, a diabetic cardiomyopathy model was induced by a single intraperitoneal injection of streptozotocin (STZ) in male Sprague Dawley rats. Diabetic rats were treated with fasudil or placebo for 8 weeks. We found that long-term administration of fasudil, a specific Rho kinase inhibitor, significantly ameliorated diabetes-induced contractile dysfunction both at cellular and whole organ levels. Fasudil-treated rats displayed improved diastolic intracellular calcium ([Ca KEY MESSAGE: Overactivation of RhoA/ROCK plays a key role in the development of DCM. Inhibition of ROCK activity with fasudil improved [Ca
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