Pre-treatment of a single high-dose of atorvastatin provided cardioprotection in different ischaemia/reperfusion models via activating mitochondrial KATP channel

Zhao, Zhigang; Cui, Wei; Zhang, Hailin; Gao, Huile; Li, Xuze; Wang, Yuanyuan; Hu, Haijuan; Li, Bo

doi:10.1016/j.ejphar.2015.01.036

Cited by 20 publications

(11 citation statements)

References 36 publications

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“…An observational clinical cohort study of breast cancer patients treated with anthracyclines suggested that statins could also reduce the risk of HF [70]. This finding appears consistent with the hitherto known cardioprotective effects of statins, such as the activation of nitric oxide synthase [71] and the opening of mitochondrial ATP-sensitive potassium channels [72]. The protective effects of statins are nonetheless most evident in patients who receive other cardiovascular drugs for preexisting risk factors.…”

Section: Primary Prevention Of Anthracycline Cardiotoxicitysupporting

confidence: 67%

Primary Prevention Strategies for Anthracycline Cardiotoxicity: A Brief Overview

Menna¹,

Salvatorelli

2017

Chemotherapy

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The clinical use of doxorubicin and other antitumor anthracyclines is limited by a dose-related risk of cardiomyopathy and heart failure which may occur “on treatment” or any time, from months to years, after completing chemotherapy. Dose reductions diminish the incidence of cardiac events attributable to anthracyclines, but heart failure still occurs in some patients exposed to low or moderate anthracycline doses. Because anthracyclines improve the life expectancy of patients with, for example, breast cancer or lymphomas, preventing or diminishing the risk of early or delayed cardiotoxicity is of obvious clinical importance. Here, we briefly review some potential strategies of primary prevention that are based on what we know about the molecular mechanisms of cardiotoxicity, and what can be done, or might be done, to interfere with the pharmacokinetic, pharmacodynamic, and genetic determinants of cardiotoxicity.

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Section: Primary Prevention Of Anthracycline Cardiotoxicitysupporting

confidence: 67%

Primary Prevention Strategies for Anthracycline Cardiotoxicity: A Brief Overview

Menna¹,

Salvatorelli

2017

Chemotherapy

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“…Moreover, preservation of mitochondrial morphology via IPC has been previously shown to confer cardioprotection in the setting of IRI 11,38–40 . Although IPC has been suggested to preserve the function of SSM mitochondria following IR, we did not observe any IPC-induced preservation of SSM mitochondria morphology following ischemia-only treatment 30,31 .…”

Section: Resultsmentioning

confidence: 99%

Unique morphological characteristics of mitochondrial subtypes in the heart: the effect of ischemia and ischemic preconditioning

Kalkhoran

Munro

Fan

et al. 2017

Discoveries (Craiova)

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Rationale Three subsets of mitochondria have been described in adult cardiomyocytes - intermyofibrillar (IMF), subsarcolemmal (SSM), and perinuclear (PN). They have been shown to differ in physiology, but whether they also vary in morphological characteristics is unknown. Ischemic preconditioning (IPC) is known to prevent mitochondrial dysfunction induced by acute myocardial ischemia/reperfusion injury (IRI), but whether IPC can also modulate mitochondrial morphology is not known. Aims Morphological characteristics of three different subsets of adult cardiac mitochondria along with the effect of ischemia and IPC on mitochondrial morphology will be investigated. Methods Mouse hearts were subjected to the following treatments (N=6 for each group): stabilization only, IPC (3x5 min cycles of global ischemia and reperfusion), ischemia only (20 min global ischemia); and IPC and ischemia. Hearts were then processed for electron microscopy and mitochondrial morphology was assessed subsequently. Results In adult cardiomyocytes, IMF mitochondria were found to be more elongated and less spherical than PN and SSM mitochondria. PN mitochondria were smaller in size when compared to the other two subsets. SSM mitochondria had similar area to IMF mitochondria but their sphericity measures were similar to PN mitochondria. Ischemia was shown to increase the sphericity parameters of all 3 subsets of mitochondria; reduce the length of IMF mitochondria, and increase the size of PN mitochondria. IPC had no effect on mitochondrial morphology either at baseline or after ischemia. Conclusion The three subsets of mitochondria in the adult heart are morphologically different. IPC does not appear to modulate mitochondrial morphology in adult cardiomyocytes.

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“…A large number of studies have confirmed that the main mechanism of reperfusion injury is oxidative stress injury caused by excessive production of free radicals and direct cell injury caused by intracellular calcium overload, along with some other potential causes, such as inflammation, microvascular injury, and endothelial dysfunction. Among these factors, oxidative stress and apoptosis play important roles in I/R injury of AMI . In the early stage of I/R injury of MI, we analysed and identified hundreds of differentially expressed lncRNAs based on previous microarray analysis .…”

Section: Discussionmentioning

confidence: 99%

“…After PCI operation, ischemic myocardial tissue regains blood supply, which saves the dying myocardial cells and greatly reduces the disability and mortality of MI patients . However, PCI treatment cannot reduce or restore the ischemic damage to myocardial cells but aggravates the degree of myocardial injury in some AMI patients . Numerous studies have confirmed that oxidative stress and cell apoptosis play an important role in this pathological process .…”

Section: Introductionmentioning

confidence: 99%

Inhibition of the LncRNA Gpr19 attenuates ischemia‐reperfusion injury after acute myocardial infarction by inhibiting apoptosis and oxidative stress via the miR‐324‐5p/Mtfr1 axis

et al. 2019

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Reperfusion therapy after acute myocardial infarction (AMI) can effectively restore the blood supply and nutritional support of ischemic myocardium and save the dying myocardium. However, myocardial ischaemia‐reperfusion (I/R) injury has become a new threat to reperfusion therapy for AMI. Many long‐chain noncoding RNAs (lncRNAs) are dysregulated by I/R damage. Of these dysregulated lncRNAs, Gpr19 was selected as a potential gene of interest based on its high expression change. We aimed to explore the functional role and molecular mechanism of Gpr19 in I/R injury of AMI. C57BL/6 mice underwent I/R injury as in vivo models. Neonatal rat ventricular cardiomyocytes (NRCMs) exposed to an oxygen glucose deprivation/recovery (OGD/R) system were used as an in vitro model. A TUNEL assay, western blot, and oxidative stress analysis were conducted in this study to determine apoptosis and oxidative stress levels. Our results indicated that inhibition of Gpr19 improves cardiac function and reduces apoptosis and myocardial fibrosis scar formation in vivo. Suppression of Gpr19 attenuates oxidative stress and apoptosis in NRCMs exposed to OGD/R. We further demonstrated that inhibition of Gpr19 decreases oxidative stress and apoptosis in OGD/R‐induced NRCMs by regulating miR‐324‐5p and mitochondrial fission regulator 1 (Mtfr1). We elucidated the functional role and potential molecular mechanism of Gpr19 in I/R injury of AMI, provided a theoretical basis for the importance of Gpr9 in I/R injury, and provided a new perspective for the clinical treatment of I/R injury of AMI.

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Pre-treatment of a single high-dose of atorvastatin provided cardioprotection in different ischaemia/reperfusion models via activating mitochondrial KATP channel

Cited by 20 publications

References 36 publications

Primary Prevention Strategies for Anthracycline Cardiotoxicity: A Brief Overview

Primary Prevention Strategies for Anthracycline Cardiotoxicity: A Brief Overview

Unique morphological characteristics of mitochondrial subtypes in the heart: the effect of ischemia and ischemic preconditioning

Inhibition of the LncRNA Gpr19 attenuates ischemia‐reperfusion injury after acute myocardial infarction by inhibiting apoptosis and oxidative stress via the miR‐324‐5p/Mtfr1 axis

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