ArticleCardiovascular research2015
Mitochondrial complex I defect and increased fatty acid oxidation enhance protein lysine acetylation in the diabetic heart.
Article in Cardiovascular research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 91 citations in OpenAlex.
- Early Cardiomyopathy in Prediabetic NDPK-B-Deficient Mice Is Associated with Remodeling of the Mitochondrial O-GlcNAc Proteome.International journal of molecular sciences · 2026Article
- Research Progress on Downstream Mechanisms of Glucose Metabolic Reprogramming and Its Role in the Occurrence and Progression of Type 2 Diabetes Mellitus.Biomedicines · 2026Review
- GCN5L1-Mediated Lysine Acetylation Regulates Mitochondrial Bioenergetics and Redox Homeostasis in the Aged Heart.Antioxidants (Basel, Switzerland) · 2026Article
- Article
- Effects of exercise training on oxidative phosphorylation-related genes in a diabetic heart via microarray analysis.BMC cardiovascular disorders · 2026Article
- Targeting the sirtuin 6-NF-κB p65 axis by 6-hydroxyhyoscyamine hydrobromide: a deacetylation-driven new therapy for diabetic wounds.Cellular & molecular biology letters · 2026Article
- Role of Antioxidants in Diseases and its Impact on Mitochondria with A Focus on Diabetes: An Overview.Current drug research reviews · 2026Review
- Article
- Influence of diet-induced obesity and voluntary exercise training on cardiac lipids and mitochondrial function in mice.Journal of sport and health science · 2025Article
- NADMetabolites · 2025Article
- Mitochondrial ultrastructural pathology in diabetic cardiomyopathy: integrated analysis via scanning electron microscopy and 3D visualization imaging.Cardiovascular diabetology · 2025Article
- Major Oxidative and Antioxidant Mechanisms During Heat Stress-Induced Oxidative Stress in Chickens.Antioxidants (Basel, Switzerland) · 2025Review
- Recent advances associated with cardiometabolic remodeling in diabetes-induced heart failure.American journal of physiology. Heart and circulatory physiology · 2024Review
- Modulation of the Cardiovascular Risk in Type 1 Diabetic Rats by Endurance Training in Combination with the Prebiotic Xylooligosaccharide.International journal of molecular sciences · 2024Article
- Amyloid beta 42 alters cardiac metabolism and impairs cardiac function in male mice with obesity.Nature communications · 2024Article
- Protein lysine acetylation does not contribute to the high rates of fatty acid oxidation seen in the post-ischemic heart.Scientific reports · 2024Article
- The role of acetylation in obesity-induced cardiac metabolic alterations.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2024Review
- Inactivation of mitochondrial MUL1 E3 ubiquitin ligase deregulates mitophagy and prevents diet-induced obesity in mice.Frontiers in molecular biosciences · 2024Article
- Diabetes Primes Neutrophils for Neutrophil Extracellular Trap Formation through Trained Immunity.Research (Washington, D.C.) · 2024Article
- WTAP boosts lipid oxidation and induces diabetic cardiac fibrosis by enhancing AR methylation.iScience · 2023Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
aimsCardiomyopathy is a major complication of diabetes. Our study was aimed to identify the sites of mitochondrial dysfunction and delineate its consequences on mitochondrial metabolism in a model of type 1 diabetes. METHODS AND
resultsDiabetes was induced by streptozotocin injection to male Lewis rats. We found a decrease in mitochondrial biogenesis pathway and electron transport chain complex assembly that targets Complex I. Oxidation of Complex II and long-chain fatty acid substrates support the electron leak and superoxide production. Mitochondrial defects do not limit fatty acid oxidation as the heart's preferred energy source indicating that the diabetic heart has a significant reserve in Complex I- and II-supported ATP production. Both mitochondrial fatty acid oxidation and Complex I defect are responsible for increased protein lysine acetylation despite an unchanged amount of the NAD(+)-dependent mitochondrial deacetylase sirt3. We quantitatively analysed mitochondrial lysine acetylation post-translational modifications and identified that the extent of lysine acetylation on 54 sites in 22 mitochondrial proteins is higher in diabetes compared with the same sites in the control. The increased lysine acetylation of the mitochondrial trifunctional protein subunit α may be responsible for the increased fatty acid oxidation in the diabetic heart.
conclusionWe identified the specific defective sites in the electron transport chain responsible for the decreased mitochondrial oxidative phosphorylation in the diabetic heart. Mitochondrial protein lysine acetylation is the common consequence of both increased fatty acid oxidation and mitochondrial Complex I defect, and may be responsible for the metabolic inflexibility of the diabetic heart.
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