ArticleOxidative medicine and cellular longevity2022
Soluble Epoxide Hydrolase Inhibition Protected against Diabetic Cardiomyopathy through Inducing Autophagy and Reducing Apoptosis Relying on Nrf2 Upregulation and Transcription Activation.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- AUDA suppresses apoptosis of HCAECs induced by TNF and serum of Kawasaki disease patients by inhibiting endoplasmic reticulum stress.Open life sciences · 2026Article
- Disturbance of Oxylipin Metabolism Mediated by Autophagy of Mesenteric Adipocytes Orchestrates Gut Inflammation in Crohn's Disease.Cellular and molecular gastroenterology and hepatology · 2026Article
- Ferroptosis: A novel therapeutic target for diabetic cardiomyopathy.World journal of diabetes · 2025Review
- Molecular mechanism on autophagy associated cardiovascular dysfunction inFrontiers in cell and developmental biology · 2025Review
- The role of Nrf2 signaling pathway in diabetic cardiomyopathy: from pathogenesis to traditional Chinese medicine interventions.Frontiers in cardiovascular medicine · 2025Review
- The role of IFI16 in regulating PANoptosis and implication in heart diseases.Cell death discovery · 2024Review
- Oxidative stress signaling in the pathogenesis of diabetic cardiomyopathy and the potential therapeutic role of antioxidant naringenin.Redox report : communications in free radical research · 2023Review
- The Beneficial and Adverse Effects of Autophagic Response to Caloric Restriction and Fasting.Advances in nutrition (Bethesda, Md.) · 2023Review
- Gene Polymorphism and Recurrent Atrial Fibrillation after Catheter Ablation: A Comprehensive Review.Reviews in cardiovascular medicine · 2023Review
- TPPU inhibits inflammation-induced excessive autophagy to restore the osteogenic differentiation potential of stem cells and improves alveolar ridge preservation.Scientific reports · 2023Article
- CYP450 Epoxygenase Metabolites, Epoxyeicosatrienoic Acids, as Novel Anti-Inflammatory Mediators.Molecules (Basel, Switzerland) · 2022Review
- Activation of Nrf2 signaling: A key molecular mechanism of protection against cardiovascular diseases by natural products.Frontiers in pharmacology · 2022Review
- Modified Linggui Zhugan Decoction protects against ventricular remodeling through ameliorating mitochondrial damage in post-myocardial infarction rats.Frontiers in cardiovascular medicine · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Many patients with diabetes die from diabetic cardiomyopathy (DCM); however, effective strategies for the prevention or treatment of DCM have not yet been clarified. Methods: Leptin receptor-deficient (db/db) mice were treated with either the soluble epoxide hydrolase (sEH) inhibitor AUDA or vehicle alone. A virus carrying Nrf2 shRNA was used to manipulate Nrf2 expression in db/db mice. Cardiac structures and functions were analyzed using echocardiography and hemodynamic examinations. Primary cardiomyocytes cultured under high glucose and high fat (HGHF) conditions were used to conduct Results: The sEH inhibitor AUDA significantly attenuated ventricular remodeling and ameliorated cardiac dysfunction in db/db mice. Interestingly, AUDA upregulated Nrf2 expression and promoted its nuclear translocation in db/db mice and the HGHF-treated cardiomyocytes. Additionally, AUDA increased autophagy and decreased apoptosis in db/db mice heart. Furthermore, the administration of AUDA promoted autophagic flux and elevated LC3-II protein level in the presence of bafilomycin A1. However, AUDA-induced autophagy was abolished, and the antiapoptotic effect was partially inhibited upon Nrf2 knockdown. Conclusion: Our findings suggest that the sEH inhibitor AUDA attenuates cardiac remodeling and dysfunction in DCM via increasing autophagy and reducing apoptosis, which is relevant to activate Nrf2 signaling pathway.
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