Inhibition of RhoA/Rho kinase by ibuprofen exerts cardioprotective effect on isoproterenol induced myocardial infarction in rats

Patel, P; Parikh, Mihir; Shah, Hital; Gandhi, Tejal

doi:10.1016/j.ejphar.2016.08.015

Cited by 18 publications

(15 citation statements)

References 24 publications

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“…Decreased cardiac apoptosis is detected in the cardiac-specific ROCK2 knockout mice [28]. Furthermore, ROCK inhibitors have been proven to have anti-apoptotic effects in myocardium and significantly improve the impaired cardiac function after pressure-overload or ischemic injury challenges [35–38]. Our lab previously found that when the endogenous ROCK1 inhibitor RhoE was deficient in mice, ROCK1 activity was increased in the hearts in response to TAC-induced pressure-overload.…”

Section: Rho Kinase and Cardiac Apoptosismentioning

confidence: 99%

Rho kinase signaling and cardiac physiology

Dai

Luo

Chang

2018

Current Opinion in Physiology

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Rho kinases (ROCKs) are the first discovered RhoA effectors that are now widely known for their effects on actin organization. Recent studies have shown that ROCKs play important roles in cardiac physiology. Abnormal activation of ROCKs participate in multiple cardiovascular pathological processes, including cardiac hypertrophy, apoptosis, fibrosis, systemic hypertension, and pulmonary hypertension. ROCK inhibitors, fasudil and statins, have shown beneficial cardiovascular effects in many animal studies, clinical trials, and applications. Here, we mainly discuss the current understanding of the physiological roles of Rho kinase signaling in the heart, and briefly summarize the roles of ROCKs in cardiac-related vascular dysfunctions. We will also discuss the clinical application of ROCK inhibitors.

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Section: Rho Kinase and Cardiac Apoptosismentioning

confidence: 99%

Rho kinase signaling and cardiac physiology

Dai

Luo

Chang

2018

Current Opinion in Physiology

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“…The role of small GTPases in the development of cardiovascular diseases is described [23] . In model animals with ischemia-reperfusion injury inhibitors of RhoA/ROCK signaling pathway demonstrate cardioprotective effect , which is realized through activation of MAPK and NFkB signaling pathways and reduction of Bcl-2 levels leading to a decrease in apoptotic activity of cells [24][25][26][27][28] .…”

Section: Resultsmentioning

confidence: 99%

From miRNA target gene network to miRNA function: miR-375 might regulate apoptosis and actin dynamics in the heart muscle via Rho-GTPases-dependent pathways

Osmak

Kiselev

Baulina

et al. 2020

Preprint

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MicroRNAs (miRNAs) are short single-stranded non-coding RNA molecules, which are involved in regulation of main biological processes, such as apoptosis, cell proliferation and differentiation, through sequence-specific interaction with target mRNAs. In this study we propose a workflow for predicting miRNAs function by analyzing the structure of the network of their target genes. This workflow was applied to study the functional role of miR-375 in the heart muscle (myocardium), since this miRNA was previously shown to be associated with heart diseases and data on its function in myocardium are mostly unclear. We identified PIK3CA, RHOA, MAPK3, PAFAH1B1, CTNNB1, MYC, PRKCA, ERBB2, and CDC42 as key genes in the miR-375 regulated network and predicted the possible function of miR-375 in the heart muscle, consisting mainly in the regulation of the Rho-GTPases-dependent signalling pathways. We implemented our algorithm for miRNA function prediction into Python module, which is available at GitHub (https://github.com/GJOsmak/miRNET).

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“…In many circumstances, myocardial ischemia results from the combined effects of increased oxygen demand and reduced amounts of oxygen. ISO, a systemic b-adrenergic receptor agonist, is associated with marked ventricular myocardial ischemia (Patel et al, 2016;Song et al, 2016), hypertrophy (Zhang et al, 2015) and fibrosis (Ma et al, 2017). Merino reported that ISO increases both atrial frequency and contractility (Merino et al, 2015), suggesting that ISO may affect the atrium.…”

Section: Discussionmentioning

confidence: 99%

Isoproterenol Increases Left Atrial Fibrosis and Susceptibility to Atrial Fibrillation by Inducing Atrial Ischemic Infarction in Rats

et al. 2020

Front. Pharmacol.

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Left atrial (LA) fibrosis is a major arrhythmogenic substrate for atrial fibrillation (AF). The purpose of this study was to assess whether isoproterenol (ISO) induces LA fibrosis and increases susceptibility to AF, exploring the underlying mechanisms. Male Sprague-Dawley rats were subcutaneously injected ISO once per day for 2 days. Five weeks after injection, the ISO group had higher susceptibility AF and prolonged AF duration compared with the control group. ISO decreased LA conduction velocity (CV) and increased LA conduction heterogeneity. ISO increased fibrosise areas and the protein levels of collagen types I and III in the left atrium. Antifibrosis drug pirfenidone decreased AF occurrence and reduced LA fibrosis in ISO treated rats. ISO injection induced atrial ischemia infarction by increasing heart rate and decreasing diastolic and systolic blood pressures. These findings demonstrated that ISO increases susceptibility to AF by increasing LA fibrosis and LA conduction abnormalities 5 weeks after injection. ISO injection induces atrial ischemic injury is the main cause of fibrosis. Rats with ISO-induced LA fibrosis may be used in further AF research.

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Inhibition of RhoA/Rho kinase by ibuprofen exerts cardioprotective effect on isoproterenol induced myocardial infarction in rats

Cited by 18 publications

References 24 publications

Rho kinase signaling and cardiac physiology

Rho kinase signaling and cardiac physiology

From miRNA target gene network to miRNA function: miR-375 might regulate apoptosis and actin dynamics in the heart muscle via Rho-GTPases-dependent pathways

Isoproterenol Increases Left Atrial Fibrosis and Susceptibility to Atrial Fibrillation by Inducing Atrial Ischemic Infarction in Rats

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