STVNa Attenuates Isoproterenol-Induced Cardiac Hypertrophy Response through the HDAC4 and Prdx2/ROS/Trx1 Pathways

Liu, Fei; Su, Hao; Liu, Bo; Mei, Ying; Ke, Qingjin; Sun, Xiaoou; Tan, Wen

doi:10.3390/ijms21020682

Cited by 19 publications

(12 citation statements)

References 43 publications

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“…22,23 In addition, our previous studies also demonstrated that STVNa significantly inhibited H9c2 cell and rat primary cardiomyocyte cell surface, restored MMP and morphological integrity, and decreased the expression of mitochondrial function-related proteins fission 1 and dynamin-related protein 1. 24 Therefore, from what has been discussed above, STVNa may be more targets for drugs. On the other hand, STVNa improved the heart function by increasing cardiac contractility and decreasing cardiac stiffness without changing intracellular Ca 2+ concentration or increasing oxygen requirement.…”

Section: Discussionmentioning

confidence: 95%

“…For instance, Isosteviol ameliorates diabetic cardiomyopathy in rats by inhibiting ERK signalling pathways and inhibit the production of reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) 22,23 . In addition, our previous studies also demonstrated that STVNa significantly inhibited H9c2 cell and rat primary cardiomyocyte cell surface, restored MMP and morphological integrity, and decreased the expression of mitochondrial function‐related proteins fission 1 and dynamin‐related protein 1 24 . Therefore, from what has been discussed above, STVNa may be more targets for drugs.…”

Section: Discussionmentioning

confidence: 97%

“…It is widely known for its sweet taste and effects on the cardiovascular system in traditional medicines of South America 19 . Several studies have reported that isosteviol possesses a cardioprotective effect in ischaemia‐reperfusion heart injuries, protects the heart against isoproterenol‐induced cardiac hypertrophy and reduces arrhythmia 20‐24 . However, whether isosteviol has a protective effect on pressure overload‐induced pathological cardiac hypertrophy has not yet been investigated.…”

Section: Introductionmentioning

confidence: 99%

“…19 Several studies have reported that isosteviol possesses a cardioprotective effect in ischaemia-reperfusion heart injuries, protects the heart against isoproterenol-induced cardiac hypertrophy and reduces arrhythmia. [20][21][22][23][24] However, whether isosteviol has a protective effect on pressure overload-induced pathological cardiac hypertrophy has not yet been investigated. STVNa is the sodium salt of isosteviol and has better water solubility than isosteviol.…”

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confidence: 99%

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The protective effect of isosteviol sodium on cardiac function and myocardial remodelling in transverse aortic constriction rat

Liu

Tang

et al. 2020

J Cellular Molecular Medi

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Cardiac hypertrophy is a compensatory response to pressure overload and a key risk factor for heart failure. 1-3 The cardiac function generally becomes deteriorative during the transition from compensated to decompensated cardiac hypertrophy. 4,5 The cardiac remodelling characterized by cardiac fibrosis that significantly reduces cardiac function and electrophysiological remodelling also occurs during the cardiac hypertrophy. 6-9 The process of cardiac hypertrophy is also accompanied by abnormal electrophysiological performance, which has a regulatory effect on cardiac isotropy. 10,11 Preventing pathological cardiac hypertrophy is a significant therapeutic goal that can postpone the progression of heart failure. 12 The aim of current pharmacotherapies such as diuretics and

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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The protective effect of isosteviol sodium on cardiac function and myocardial remodelling in transverse aortic constriction rat

Liu

Tang

et al. 2020

J Cellular Molecular Medi

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“…Isosteviol (IST) is a bioactive diterpenoid extracted by Stevia rebaudiana that has a variety of biological activities targeted at the CVS, including anti-hypertensive, anti-hyperglycemic, antioxidant, and anti-inflammatory effects [ 129 ]. In cardiomyoblasts subjected to simulated IR or pro-hypertrophic injuries, IST restored mitochondrial membrane potential, morphological integrity, and biogenesis; decreased ROS levels; and upregulated the expression of antioxidant enzymes [ 130 , 131 ]. In addition, IST relieved IR injury in rodent hearts and isolated pig hearts [ 132 , 133 ].…”

Section: Mitochondria-targeting Of Natural Compounds With Pleiotromentioning

confidence: 99%

Mitochondria-Targeted Drug Delivery in Cardiovascular Disease: A Long Road to Nano-Cardio Medicine

et al. 2020

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Cardiovascular disease (CVD) represents a major threat for human health. The available preventive and treatment interventions are insufficient to revert the underlying pathological processes, which underscores the urgency of alternative approaches. Mitochondria dysfunction plays a key role in the etiopathogenesis of CVD and is regarded as an intriguing target for the development of innovative therapies. Oxidative stress, mitochondrial permeability transition pore opening, and excessive fission are major noxious pathways amenable to drug therapy. Thanks to the advancements of nanotechnology research, several mitochondria-targeted drug delivery systems (DDS) have been optimized with improved pharmacokinetic and biocompatibility, and lower toxicity and antigenicity for application in the cardiovascular field. This review summarizes the recent progress and remaining obstacles in targeting mitochondria as a novel therapeutic option for CVD. The advantages of nanoparticle delivery over un-targeted strategies are also discussed.

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Isoproterenol mechanisms in inducing myocardial fibrosis and its application as an experimental model for the evaluation of therapeutic potential of phytochemicals and pharmaceuticals

Bader Eddin,

Nagoor Meeran,

Kumar Jha

et al. 2024

Anim Models and Exp Med

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Cardiac injury initiates repair mechanisms and results in cardiac remodeling and fibrosis, which appears to be a leading cause of cardiovascular diseases. Cardiac fibrosis is characterized by the accumulation of extracellular matrix proteins, mainly collagen in the cardiac interstitium. Many experimental studies have demonstrated that fibrotic injury in the heart is reversible; therefore, it is vital to understand different molecular mechanisms that are involved in the initiation, progression, and resolution of cardiac fibrosis to enable the development of antifibrotic agents. Of the many experimental models, one of the recent models that has gained renewed interest is isoproterenol (ISP)–induced cardiac fibrosis. ISP is a synthetic catecholamine, sympathomimetic, and nonselective β‐adrenergic receptor agonist. The overstimulated and sustained activation of β‐adrenergic receptors has been reported to induce biochemical and physiological alterations and ultimately result in cardiac remodeling. ISP has been used for decades to induce acute myocardial infarction. However, the use of low doses and chronic administration of ISP have been shown to induce cardiac fibrosis; this practice has increased in recent years. Intraperitoneal or subcutaneous ISP has been widely used in preclinical studies to induce cardiac remodeling manifested by fibrosis and hypertrophy. The induced oxidative stress with subsequent perturbations in cellular signaling cascades through triggering the release of free radicals is considered the initiating mechanism of myocardial fibrosis. ISP is consistently used to induce fibrosis in laboratory animals and in cardiomyocytes isolated from animals. In recent years, numerous phytochemicals and synthetic molecules have been evaluated in ISP‐induced cardiac fibrosis. The present review exclusively provides a comprehensive summary of the pathological biochemical, histological, and molecular mechanisms of ISP in inducing cardiac fibrosis and hypertrophy. It also summarizes the application of this experimental model in the therapeutic evaluation of natural as well as synthetic compounds to demonstrate their potential in mitigating myocardial fibrosis and hypertrophy.

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STVNa Attenuates Isoproterenol-Induced Cardiac Hypertrophy Response through the HDAC4 and Prdx2/ROS/Trx1 Pathways

Cited by 19 publications

References 43 publications

The protective effect of isosteviol sodium on cardiac function and myocardial remodelling in transverse aortic constriction rat

The protective effect of isosteviol sodium on cardiac function and myocardial remodelling in transverse aortic constriction rat

Mitochondria-Targeted Drug Delivery in Cardiovascular Disease: A Long Road to Nano-Cardio Medicine

Isoproterenol mechanisms in inducing myocardial fibrosis and its application as an experimental model for the evaluation of therapeutic potential of phytochemicals and pharmaceuticals

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