Statins protect against arrhythmogenic calcium alternans in the post–myocardial infarction diabetic heart: Pleiotropy on steroids

Verrier, Richard L.

doi:10.1016/j.hrthm.2017.06.010

Cited by 3 publications

(2 citation statements)

References 14 publications

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“…Statins protect against arrhythmogenic calcium alternans in the post-myocardial infarction diabetic heart ( 17 ). Statins induce sirtuin 1 protein and have a cardioprotective role following premature myocardial infarction by impairment of endothelial nitric oxide synthase expression ( 18 ).…”

Section: Introductionmentioning

confidence: 99%

Statin rosuvastatin inhibits apoptosis of human coronary artery endothelial cells through upregulation of the JAK2/STAT3 signaling pathway

Wang¹,

Li²,

Xie³

et al. 2020

Mol Med Rep

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The purpose of the present study was to explore the potential molecular signaling pathway mediated by the statin rosuvastatin in cultured human coronary artery endothelial cells (Hcaecs) induced by cocl 2. cocl 2 was used to induce the apoptosis of Hcaecs. Myocardial infarction rats were established and received statin or PBS treatment. reverse transcription-quantitative Pcr, western blotting, eliSa, Tunel assay and immunohistochemistry were used to analyze the role of statin treatment. The results showed that rosuvastatin treatment decreased apoptosis of Hcaecs induced by cocl 2 by increasing anti-apoptosis Bcl-xl and Bcl-2 expression, and decreasing pro-apoptosis Bax, Bad, caspase-3 and caspase-9 expression. The myocardial ischemia rat model demonstrated that rosuvastatin treatment decreased the mitochondrial reactive oxygen species, inflammation, mitochondrial damage, lipid catabolism, heart failure and the myocardial infarction areas, but improved the cardiac function indicators, right and left ventricular ejection fraction and increased expression levels of Janus kinase (JaK) and signal transducer and activator of transcription (STaT)3 in myocardial tissue. in conclusion, the results of the current study revealed that the statin rosuvastatin presents cardioprotective effects by activation of the JaK2/STaT3 signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Statin rosuvastatin inhibits apoptosis of human coronary artery endothelial cells through upregulation of the JAK2/STAT3 signaling pathway

Wang¹,

Li²,

Xie³

et al. 2020

Mol Med Rep

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show abstract

“…Statins can be used for venous thromboembolism, 22,23 cancers, 24 stroke, [25][26][27]31 and even as an antiarrhythmic drug. [28][29][30] However, statins have already been proven to reduce stroke risk and atherosclerosis mainly by reducing low-density lipoprotein cholesterol, which is exactly the effect of hypolipidemic agents and not by reducing inflammation. 31 In our study, we cannot determine which pharmacological mechanism was involved in the reduction of COPD exacerbation and mortality rates by statins.…”

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confidence: 99%

Association Between Statin Use and Exacerbation of Chronic Obstructive Pulmonary Disease Among Patients Receiving Corticosteroids

Huang

Kao

Chian

et al. 2021

COPD

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Purpose The role of statins as anti-inflammatory drugs in chronic obstructive pulmonary disease (COPD) is controversial. This study aimed to determine the efficacy of statins used with or without corticosteroids in COPD patients. Patients and Methods This was a retrospective cohort study and used the two million outpatients and inpatients in Taiwan’s Longitudinal Health Insurance Database covering 2000 to 2015. A total of 92,460 patients were identified in this study. We divided COPD patients into four groups by auditing each patient’s medication (statins used or not; corticosteroids used or not) and used Cox regression to analyze and compare the effects of statins in COPD patients with or without corticosteroids. Results In terms of all COPD patients, our findings were consistent with previous studies showing that statins decreased COPD-related hospitalization and mortality rates. However, the beneficial effects were only observed in younger patients or those not taking corticosteroids in further analysis. Statins significantly decreased hospitalization and mortality rates in the non-corticosteroids groups. The hazard ratios increased with age and were not statistically significant for patients > 70 years old. Statins did not significantly decrease ED visits, hospitalization, and mortality in corticosteroids groups. Conclusion Statins decreased hospitalization and mortality rates in COPD patients not taking corticosteroids but were not efficacious in patients on corticosteroids therapy. Furthermore, the beneficial effects of statins gradually decreased with patient age. Based on the findings, statins used in COPD patients may need to consider the patient age and corticosteroids used or not.

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Single Bolus Rosuvastatin Accelerates Calcium Uptake and Attenuates Conduction Inhomogeneity in Failing Rabbit Hearts With Regional Ischemia–Reperfusion Injury

Chou

Lee

Huang

et al. 2020

Journal of Cardiovascular Pharmacology

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Acute statin therapy reduces myocardial ischemia/reperfusion (IR) injury–induced ventricular fibrillation (VF), but the underlying electrophysiological mechanisms remain unclear. This study sought to investigate the antiarrhythmic effects of a single bolus rosuvastatin injection in failing rabbit hearts with IR injury and to unveil the underlying molecular mechanisms. Rabbits were divided into rosuvastatin, rosuvastatin + l-NAME, control, and l-NAME groups. Intravenous bolus rosuvastatin (0.5 mg/kg) and/or l-NAME (10 mg/kg) injections were administered 1 hour and 15 minutes before surgery, respectively. Heart failure was induced using rapid ventricular pacing. Under general anesthesia with isoflurane, an IR model was created by coronary artery ligation for 30 minutes, followed by reperfusion for 15 minutes. Plasma NO end product levels were measured during IR. Then, hearts were excised and Langendorff-perfused for optical mapping studies. Cardiac tissues were sampled for Western blot analysis. Rosuvastatin increased plasma NO levels during IR, which was abrogated by l-NAME. Spontaneous VF during IR was suppressed by rosuvastatin (P < 0.001). Intracellular calcium (Cai) decay and conduction velocity were significantly slower in the IR zone. Rosuvastatin accelerated Cai decay, ameliorated conduction inhomogeneity, and reduced the inducibility of spatially discordant alternans and VF significantly. Western blots revealed significantly higher expression of enhancing endothelial NO-synthase and phosphorylated enhancing endothelial NO-synthase proteins in the Rosuvastatin group. Furthermore, SERCA2a, phosphorylated connexin43, and phosphorylated phospholamban were downregulated in the IR zone, which was attenuated or reversed by rosuvastatin. Acute rosuvastatin therapy before ischemia reduced IR-induced VF by improving SERCA2a function and ameliorating conduction disturbance in the IR zone.

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Statins protect against arrhythmogenic calcium alternans in the post–myocardial infarction diabetic heart: Pleiotropy on steroids

Cited by 3 publications

References 14 publications

Statin rosuvastatin inhibits apoptosis of human coronary artery endothelial cells through upregulation of the JAK2/STAT3 signaling pathway

Statin rosuvastatin inhibits apoptosis of human coronary artery endothelial cells through upregulation of the JAK2/STAT3 signaling pathway

Association Between Statin Use and Exacerbation of Chronic Obstructive Pulmonary Disease Among Patients Receiving Corticosteroids

Single Bolus Rosuvastatin Accelerates Calcium Uptake and Attenuates Conduction Inhomogeneity in Failing Rabbit Hearts With Regional Ischemia–Reperfusion Injury

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