ArticleAntioxidants (Basel, Switzerland)2022
NADPH Oxidase Mediates Oxidative Stress and Ventricular Remodeling through SIRT3/FOXO3a Pathway in Diabetic Mice.
Article in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Liraglutide affects mitochondrial function and histone acetylation through the NQO1/SIRT3 pathway in diabetic kidney disease.Molecular and cellular biochemistry · 2026Article
- Copper peptide activated cascade catalysis for glucose regulation and hypoxia reversing in infected diabetic wound healing.Materials today. Bio · 2026Article
- Cross-regulatory mechanisms linking ferroptosis, epigenetics, and circadian rhythm to mitochondrial quality control in diabetic cardiomyopathy.Journal of advanced research · 2026Review
- SIRT3-mediated deacetylation of FoxM1 prevents pulmonary fibrosis via modulating the activation of pulmonary fibroblasts.Redox biology · 2026Article
- Empagliflozin Ameliorates Diabetic Cardiomyopathy by Inhibiting Ferroptosis via SIRT3: Mechanisms and Therapeutic Implications.Antioxidants (Basel, Switzerland) · 2026Article
- Oxidative Stress in Diabetic Cardiomyopathy: Molecular Mechanisms and Emerging Therapeutic Targets.Biomolecules · 2026Review
- Neuroinflammation and NeuroHIV: understanding the role of HIV-1 related factors in microglial activation.Translational psychiatry · 2026Review
- Endothelial ferroptosis: a novel mechanism and therapeutic target in diabetic microvascular complications.Molecular medicine (Cambridge, Mass.) · 2026Review
- Integrated Multi-Omics Analysis Identifies PDK4 and ACOT1 as Metabolic Hub Genes Associated With Myocardial Fibrosis in Diabetic Cardiomyopathy.Journal of diabetes research · 2026Article
- System biology-based assessment of the molecular mechanism of epigallocatechin gallate in Parkinson's disease: via network pharmacology, in-silico evaluation & in-vitro studies.Scientific reports · 2025Article
- Ferroptosis: A novel therapeutic target for diabetic cardiomyopathy.World journal of diabetes · 2025Review
- Mapping the future: bibliometric insights into ferroptosis and diabetic nephropathy.Frontiers in physiology · 2025Review
- Sea buckthorn flavonoids and their derivatives: potential natural compounds for the treatment of diabetic cardiomyopathy.Frontiers in pharmacology · 2025Review
- Targeting NADPH oxidase-driven oxidative stress in diabetic cardiomyopathy: mechanisms and therapeutic perspectives.Frontiers in pharmacology · 2025Review
- Iron accumulation and lipid peroxidation: implication of ferroptosis in diabetic cardiomyopathy.Diabetology & metabolic syndrome · 2023Review
- The role and mechanism of NADPH oxidase in the development and progression of thyroid carcinoma.American journal of cancer research · 2023Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Oxidative stress and mitochondrial dysfunction are important mechanisms of ventricular remodeling, predisposed to the development of diabetic cardiomyopathy (DCM) in type 2 diabetes mellitus. In this study, we have successfully established a model of type 2 diabetes using a high-fat diet (HFD) in combination with streptozotocin (STZ). The mice were divided into three groups of six at random: control, diabetes, and diabetes with apocynin and the H9c2 cell line was used as an in vitro model for investigation. We examined the molecular mechanisms of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activation on mitochondrial dysfunction and ventricular remodeling in the diabetic mouse model. Hyperglycemia-induced oxidative stress led to a reduced expression of sirtuin 3 (SIRT3), thereby promoting forkhead box class O 3a (FOXO3a) acetylation in ventricular tissue and H9c2 cells. Reactive oxygen species (ROS) overproduction promoted ventricular structural modeling and conduction defects. These alterations were mitigated by inhibiting NADPH oxidase with the pharmaceutical drug apocynin (APO). Apocynin improved SIRT3 and Mn-SOD expression in H9c2 cells transfected with SIRT3 siRNA. In our diabetic mouse model, apocynin improved myocardial mitochondrial function and ROS overproduction through the recovery of the SIRT3/FOXO3a pathway, thereby reducing ventricular remodeling and the incidence of DCM.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.