ArticleCardiovascular diabetology2015
Histone deacetylase (HDAC) inhibition improves myocardial function and prevents cardiac remodeling in diabetic mice.
Article in Cardiovascular diabetology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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Who cites it
92 citing papers in PubMed, 148 citations in OpenAlex.
- The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026Review
- Defective efferocytosis in diabetes: molecular mechanisms and emerging therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- DUSP family phosphatases in cell signaling, inflammation, and chronic diseases.Journal of biomedical science · 2026Review
- Modulation of the gut-heart axis by exercise in diabetic cardiomyopathy: Microbial mechanisms and clinical implications.iScience · 2026Review
- Exploring the basis of Traditional Chinese Medicine in treating cardiovascular disease: insights into the microbiota-gut-heart axis.Chinese medicine · 2026Review
- Role of Perturbations of Epigenetic Processes in Cardiac Hypertrophy and Fibrotic Scarring.Current cardiology reviews · 2026Review
- Role of Histone Deacetylase and Inhibitors in Cardiovascular Diseases.Cell proliferation · 2025Review
- Gut Microbiota-Derived Metabolites Orchestrate Metabolic Reprogramming in Diabetic Cardiomyopathy: Mechanisms and Therapeutic Frontiers.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Extracellular vesicles from adipose-derived mesenchymal stem cells prevent high glucose-induced retinal ganglion cell pyroptosis through a microRNA-26a-5p-dependent mechanism.Journal of diabetes investigation · 2025Article
- Cellular and Molecular Mechanisms Explaining the Link Between Inflammatory Bowel Disease and Heart Failure.Cells · 2025Review
- HDAC4: an emerging target in diabetes mellitus and diabetic complications.European journal of medical research · 2025Review
- Critical Appraisal of Pharmaceutical Therapy in Diabetic Cardiomyopathy-Challenges and Prospectives.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Sodium Butyrate, A Gut Microbiota Derived Metabolite in Type 2 Diabetes Mellitus and Cardiovascular Disease: A Review.Cardiovascular & hematological agents in medicinal chemistry · 2025Review
- Recent advancements and comprehensive analyses of butyric acid in cardiovascular diseases.Frontiers in cardiovascular medicine · 2025Review
- The role of the gut microbiota in the onset and progression of heart failure: insights into epigenetic mechanisms and aging.Clinical epigenetics · 2024Review
- Genetic deletion or pharmacologic inhibition of histone deacetylase 6 protects the heart against ischaemia/reperfusion injury by limiting tumour necrosis factor alpha-induced mitochondrial injury in experimental diabetes.Cardiovascular research · 2024Article
- Molecular Basis of Cardiomyopathies in Type 2 Diabetes.International journal of molecular sciences · 2024Review
- Review
- The protective role of endothelial GLUT1 in ischemic stroke.Brain and behavior · 2024Review
- Epigenetics in diabetic cardiomyopathy.Clinical epigenetics · 2024Review
32 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundRecent evidence indicates that inhibition of histone deacetylase (HDAC) protects the heart against myocardial injury and stimulates endogenous angiomyogenesis. However, it remains unknown whether HDAC inhibition produces the protective effect in the diabetic heart. We sought to determine whether HDAC inhibition preserves cardiac performance and suppresses cardiac remodeling in diabetic cardiomyopathy.
methodsAdult ICR mice received an intraperitoneal injection of either streptozotocin (STZ, 200 mg/kg) to establish the diabetic model or vehicle to serve as control. Once hyperglycemia was confirmed, diabetic mice received sodium butyrate (1%), a specific HDAC inhibitor, in drinking water on a daily basis to inhibit HDAC activity. Mice were randomly divided into following groups, which includes Control, Control + Sodium butyrate (NaBu), STZ and STZ + Sodium butyrate (NaBu), respectively. Myocardial function was serially assessed at 7, 14, 21 weeks following treatments.
resultsEchocardiography demonstrated that cardiac function was depressed in diabetic mice, but HDAC inhibition resulted in a significant functional improvement in STZ-injected mice. Likewise, HDAC inhibition attenuates cardiac hypertrophy, as evidenced by a reduced heart/tibia ratio and areas of cardiomyocytes, which is associated with reduced interstitial fibrosis and decreases in active caspase-3 and apoptotic stainings, but also increased angiogenesis in diabetic myocardium. Notably, glucose transporters (GLUT) 1 and 4 were up-regulated following HDAC inhibition, which was accompanied with increases of GLUT1 acetylation and p38 phosphorylation. Furthermore, myocardial superoxide dismutase, an important antioxidant, was elevated following HDAC inhibition in the diabetic mice.
conclusionHDAC inhibition plays a critical role in improving cardiac function and suppressing myocardial remodeling in diabetic heart.
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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.