ArticleEuropean journal of applied physiology2012
Fasudil, a Rho-kinase inhibitor, protects against excessive endurance exercise training-induced cardiac hypertrophy, apoptosis and fibrosis in rats.
Article in European journal of applied physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 43 citations in OpenAlex.
- Influence of Rho kinase inhibitor Fasudil on late endothelial progenitor cells in peripheral blood of COPD patients with pulmonary artery hypertension.Bosnian journal of basic medical sciences · 2014Trial
- The role of exercise in modulating NAD+ metabolic enzymes: mechanisms and health benefits.Frontiers in sports and active living · 2026Review
- Superior Antiproliferative and Enhanced Synergistic Effects of a ROCK Inhibitor in Multiple Models for Keloid Disease.JID innovations : skin science from molecules to population health · 2025Article
- The effect of endurance exercise and rosehip extract supplementation on the expression of P53 and cytochrome C genes in male rat heart.Journal of cardiovascular and thoracic research · 2022Article
- The impact of moderate endurance exercise on cardiac telomeres and cardiovascular remodeling in obese rats.Frontiers in cardiovascular medicine · 2022Article
- Exercise-induced signaling pathways to counteracting cardiac apoptotic processes.Frontiers in cell and developmental biology · 2022Review
- Left Cardiac Remodelling Assessed by Echocardiography Is Associated with Rho-Kinase Activation in Long-Distance Runners.Journal of cardiovascular development and disease · 2021Article
- Rho kinase cascade activation in circulating leukocytes in patients with diabetes mellitus type 2.Cardiovascular diabetology · 2020Observational
- Rho-kinase pathway activation and apoptosis in circulating leucocytes in patients with heart failure with reduced ejection fraction.Journal of cellular and molecular medicine · 2020Observational
- Tsantan Sumtang Restored Right Ventricular Function in Chronic Hypoxia-Induced Pulmonary Hypertension Rats.Frontiers in pharmacology · 2020Article
- FSD-C10 Shows Therapeutic Effects in Suppressing oxidized low-density lipoprotein (ox-LDL)-Induced Human Brain Microvascular Endothelial Cells Apoptosis via Rho-Associated Coiled-Coil Kinase (ROCK)/Mitogen-Activated Protein Kinase (MAPK) Signaling.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Review
- Association of physical performance and biochemical profile of mice with intrinsic endurance swimming.International journal of medical sciences · 2016Article
- Exhaustive submaximal endurance and resistance exercises induce temporary immunosuppression via physical and oxidative stress.Journal of exercise rehabilitation · 2015Article
- The Effects of Fasudil at Different Doses on Acute Myocardial Infarction in Rats.Acta Cardiologica Sinica · 2013Article
- Rho kinases in cardiovascular physiology and pathophysiology: the effect of fasudil.Journal of cardiovascular pharmacology · 2013Review
- Hepatoprotective Effects of Swimming Exercise against D-Galactose-Induced Senescence Rat Model.Evidence-based complementary and alternative medicine : eCAM · 2013Article
- Pumpkin (Cucurbita moschata) fruit extract improves physical fatigue and exercise performance in mice.Molecules (Basel, Switzerland) · 2012Article
- Cardioprotective effects of aerobic training in diabetic rats: Reducing cardiac apoptotic indices and oxidative stress for a healthier heart.ARYA atherosclerosisArticle
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive endurance exercise training (EEET) is accompanied by cardiac remodeling, changes in ventricular function and increased heart failure risk. Fasudil, a potent Rho-kinase inhibitor, has been demonstrated to blunt cardiomyocyte hypertrophy, cardiac remodeling, and heart failure progression in pre-clinical trials and has been approved for clinical use in Japan. We examined the in vivo bioefficacy of fasudil against EEET-induced cardiac remodeling and the underlying molecular mechanisms. Male Sprague-Dawley rats were randomly divided into three groups: sedentary control (SC), EEET, and EEET with fasudil treatment (EEET-F). Rats in EEET and EEET-F groups ran on a motorized treadmill for 12 weeks. The results revealed that EEET increased myocardial hypertrophy (LV weight/tibial length), myocyte cross-sectional area, hypertrophy-related pathways (IL6/STAT3-MEK5-ERK5, calcineurin-NFATc3, p38 and JNK MAPK), hypertrophic markers (ANP/BNP), pro-apoptotic molecules (cytochrome C, cleaved caspase-3 and PARP), and fibrosis-related pathways (FGF-2-ERK1/2) and fibrosis markers (uPA, MMP-9 and -2). These pathways were then expressed lower in the EEET-F group when compared with the EEET group. The cardiac hypertrophic level, apoptotic pathway and fibrosis signaling were further inhibited in the fasudil-treated group. We systematically investigated the possible signaling pathways leading to EEET-induced cardiac hypertrophy, apoptosis and fibrosis. We also provide evidence for the novel function of fasudil in suppressing EEET-induced cardiac remodeling and impairment by multiple mechanisms, which suggests that the RhoA signaling pathway contributes to EEET-induced cardiac remodeling and dysfunction.
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