ArticleCardiovascular diabetology2016
N-acetylcysteine attenuates myocardial dysfunction and postischemic injury by restoring caveolin-3/eNOS signaling in diabetic rats.
Article in Cardiovascular diabetology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 60 citations in OpenAlex.
- Role of membrane microdomains in cardiac protection: strategies for diabetic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2025Review
- Molecular Insights into Oxidative-Stress-Mediated Cardiomyopathy and Potential Therapeutic Strategies.Biomolecules · 2025Review
- Cardioprotective strategies in myocardial ischemia-reperfusion injury: Implications for improving clinical translation.Journal of molecular and cellular cardiology plus · 2025Review
- Caveolin-3: therapeutic target for diabetic myocardial ischemia/reperfusion injury.Molecular medicine (Cambridge, Mass.) · 2025Review
- Caveolin and oxidative stress in cardiac pathology.Frontiers in physiology · 2025Review
- N-acetylcysteine Protects Against Myocardial Ischemia-Reperfusion Injury Through Anti-ferroptosis in Type 1 Diabetic Mice.Cardiovascular toxicology · 2024Article
- CAV3 alleviates diabetic cardiomyopathy via inhibiting NDUFA10-mediated mitochondrial dysfunction.Journal of translational medicine · 2024Article
- Update on clinical and experimental management of diabetic cardiomyopathy: addressing current and future therapy.Frontiers in endocrinology · 2024Review
- Role of AIM2 Gene Knockdown Mechanism in Diabetic Cardiomyopathy: an In Vivo and Ex Vivo Study.Applied biochemistry and biotechnology · 2023Article
- Pharmacological treatment of type 2 diabetes in elderly patients with heart failure: randomized trials and beyond.Heart failure reviews · 2023Review
- Puerarin Attenuates High-Glucose and High-Lipid-Induced Inflammatory Injury in H9c2 Cardiomyocytes via CAV3 Protein Upregulation.Journal of inflammation research · 2023Article
- Advances in research on the protective mechanisms of traditional Chinese medicine (TCM) in myocardial ischaemia-reperfusion injury.Pharmaceutical biology · 2022Article
- Myocardial ischemia/reperfusion injury: Mechanisms of injury and implications for management (Review).Experimental and therapeutic medicine · 2022Review
- Article
- Dexmedetomidine Leads to the Mitigation of Myocardial Ischemia/Reperfusion-Induced Acute Lung Injury in Diabetic Rats Via Modulation of Hypoxia-Inducible Factor-1α.Brazilian journal of cardiovascular surgery · 2022Article
- Propionate alleviates myocardial ischemia-reperfusion injury aggravated by Angiotensin II dependent on caveolin-1/ACE2 axis through GPR41.International journal of biological sciences · 2022Article
- SUMOylation of Nuclear γ-Actin by SUMO2 supports DNA Damage Repair against Myocardial Ischemia-Reperfusion Injury.International journal of biological sciences · 2022Article
- The importance of caveolin as a target in the prevention and treatment of diabetic cardiomyopathy.Frontiers in immunology · 2022Review
- Selective inhibition of PKCβ2 improves Caveolin-3/eNOS signaling and attenuates lipopolysaccharide-induced injury by inhibiting autophagy in H9C2 cardiomyocytes.Journal of molecular histology · 2021Article
- Application of Animal Models in Diabetic Cardiomyopathy.Diabetes & metabolism journal · 2021Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPatients with diabetes are prone to develop cardiac hypertrophy and more susceptible to myocardial ischemia-reperfusion (I/R) injury, which are concomitant with hyperglycemia-induced oxidative stress and impaired endothelial nitric oxide (NO) synthase (eNOS)/NO signaling. Caveolae are critical in the transduction of eNOS/NO signaling in cardiovascular system. Caveolin (Cav)-3, the cardiomyocytes-specific caveolae structural protein, is decreased in the diabetic heart in which production of reactive oxygen species are increased. We hypothesized that treatment with antioxidant N-acetylcysteine (NAC) could enhance cardiac Cav-3 expression and attenuate caveolae dysfunction and the accompanying eNOS/NO signaling abnormalities in diabetes.
methodsControl or streptozotocin-induced diabetic rats were either untreated or treated with NAC (1.5 g/kg/day, NAC) by oral gavage for 4 weeks. Rats in subgroup were randomly assigned to receive 30 min of left anterior descending artery ligation followed by 2 h of reperfusion. Isolated rat cardiomyocytes or H9C2 cells were exposed to low glucose (LG, 5.5 mmol/L) or high glucose (HG, 25 mmol/L) for 36 h before being subjected to 4 h of hypoxia followed by 4 h of reoxygenation (H/R).
resultsNAC treatment ameliorated myocardial dysfunction and cardiac hypertrophy, and attenuated myocardial I/R injury and post-ischemic cardiac dysfunction in diabetic rats. NAC attenuated the reductions of NO, Cav-3 and phosphorylated eNOS and mitigated the augmentation of O
conclusionsHyperglycemia-induced inhibition of eNOS activity might be consequences of caveolae dysfunction and reduced Cav-3 expression. Antioxidant NAC attenuated myocardial dysfunction and myocardial I/R injury by improving Cav-3/eNOS signaling.
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