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Rosuvastatin postconditioning protects isolated hearts against ischemia–reperfusion injury: The role of radical oxygen species, PI 3K–Akt–GSK‐3β pathway, and mitochondrial permeability transition pore
Abstract
Summary: Aims: Glycogen synthase kinase‐3β (GSK‐3β) and mitochondrial permeability transition pore (mPTP) play an important role in myocardial ischemia–reperfusion injury. The aim of this study was to investigate whether postconditioning with rosuvastatin is able to reduce myocardial ischemia–reperfusion injury and clarify the potential mechanisms. Methods: Isolated rat hearts underwent 30 minutes of ischemia and 60 minutes of reperfusion in the presence or absence of rosuvastatin (1‐50 nmol/L). The activity of signaling pathway was determined by Western blot analysis, and Ca 2+‐induced mPTP opening was assessed by the use of a potentiometric method. Results: Rosuvastatin significantly reduced myocardial infarct size and improved cardiac function at 5 and 10 nmol/L. Protection disappeared at higher concentration and reverted to increased damage at 50 nmol/L. At 5 nmol/L, rosuvastatin increased the phosphorylation of protein kinase B (Akt) and GSK‐3β, concomitant with a higher Ca 2+ load required to open the mPTP. Rosuvastatin postconditioning also significantly increased superoxide dismutase activity and reduced malondialdehyde and radical oxygen species level. LY 294002, phosphatidylinositol‐3‐kinase (PI 3K) inhibitors, abolished these protective effects of rosuvastatin postconditioning. Conclusion: Rosuvastatin prevents myocardial ischemia–reperfusion injury by inducing phosphorylation of PI 3K–Akt and GSK‐3β, preventing oxidative stress and subsequent inhibition of mPTP opening.
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“The studies performed by Liu et al revealed that the reduction of circulating/intramuscular CoQ10 after statin treatment decreased the phosphorylation potential of adenosine diphosphate and the activity of mitochondrial complex I and IV, which contributes to mitochondrial dysfunction.31, 32, 33, 34”
From Effects of Coenzyme Q10 on Statin‐Induced Myopathy: An Updated Meta‐Analysis of Randomized Controlled Trials (2018) · cites this paper as [32]
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Effect of Cyclosporine on Reperfusion Injury in Acute Myocardial Infarction
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Cyclosporine before PCI in Patients with Acute Myocardial Infarction
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The mitochondrial permeability transition pore and ischemia-reperfusion injury
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Effect of Cyclosporine on Left Ventricular Remodeling After Reperfused Myocardial Infarction
Mewton, N., Croisille, P., Gahide, G., Rioufol, G., Bonnefoy‐Cudraz, E., Sanchez, I., Cung, T. T., Sportouch, C., Angoulvant, D., Finet, G., et al. (2010) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2009.10.052 · Cited by 198
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Qu, H., Guo, M., Chai, H., Wang, W., Gao, Z., & Shi, D. (2018) · Journal of the American Heart Association · doi:10.1161/jaha.118.009835 · Cited by 178
Metadata
- Authors
- Liu, C., Yang, F., Cheng, S., Liu, Y., Wan, L., & Cong, H.
- Affiliations
- Tianjin Chest Hospital (CN)
- Tianjin Medical University Cancer Institute and Hospital (CN)
- Department of Thoracic Surgery Tianjin Chest Hospital Tianjin China
- Department of Cardiology Tianjin Medical University Tianjin Chest Hospital Tianjin China
- Venue
- Cardiovascular Therapeutics
- Publisher
- Wiley
- Published
- 2016-12-13
- Volume
- 35
- Issue
- 1
- Pages
- 3-9
- ISSN
- 1755-5914 (ISSN-L)
- 1755-5922
- OpenAlex
- W2512501821
- Cited by
- 52
- References
- 28
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 3 · 2023: 1 · 2022: 5 · 2021: 9 · 2020: 7 · 2019: 6 · 2018: 9 · 2017: 7
- FWCI
- 6.65
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cardiovascular Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
- Life Sciences › Neuroscience › Neurology › Neuroprotection in Cerebral Ischemia
- Health Sciences › Medicine › Nephrology › Acute Kidney Injury Research
- Keywords
- rosuvastatin, myocardial ischemia-reperfusion injury, cardioprotection, postconditioning, GSK3β, PI3K/Akt signaling, mitochondrial permeability transition pore, oxidative stress, reactive oxygen species, superoxide dismutase, malondialdehyde, statins, myocardial infarct size, isolated rat heart
- MeSH terms
- Isolated Heart Preparation, Rosuvastatin Calcium, Glycogen Synthase Kinase 3 beta, Phosphoinositide-3 Kinase Inhibitors, Mitochondrial Permeability Transition Pore, Animals, Antioxidants, Disease Models, Animal, Dose-Response Relationship, Drug, Male, Mitochondria, Heart, Myocardial Infarction, Phosphorylation, Time Factors, Myocardial Reperfusion Injury, Ventricular Function, Left, Rats, Wistar, Reactive Oxygen Species, Oxidative Stress, Cytoprotection, Calcium Signaling, Myocytes, Cardiac, Mitochondrial Membrane Transport Proteins, Protein Kinase Inhibitors, Proto-Oncogene Proteins c-akt, Phosphatidylinositol 3-Kinase
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