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Cited by 52Cardiac Ischemia and ReperfusionNeuroprotection in Cerebral IschemiaAcute Kidney Injury Research

The DOI matches its Crossref record; 28 of the 28 references it cites were found in a registry or an index.

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

Liu, Chun‐Wei, Yang, Fan, Cheng, Shi‐Zhao, Liu, Yue, Wan, Liang‐Hui, Cong, Hong‐Liang·2017·Cardiovascular Therapeutics
DOI 10.1111/1755-5922.12225
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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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Crossref · 10.1111/1755-5922.12225

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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
ORCID
Venue
Cardiovascular Therapeutics
Publisher
Wiley
Published
2016-12-13
Volume
35
Issue
1
Pages
3-9
ISSN
  • 1755-5914 (ISSN-L)
  • 1755-5922
DOI
10.1111/1755-5922.12225
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
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
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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