ArticleActa diabetologica2018
MC1568 improves insulin secretion in islets from type 2 diabetes patients and rescues β-cell dysfunction caused by Hdac7 upregulation.
Article in Acta diabetologica, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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22 citing papers in PubMed, 40 citations in OpenAlex.
- Histone deacetylase 7 mediates lipopolysaccharide-inducible mitochondrial fission in macrophages.Journal of cell science · 2025Article
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- Harnessing Pharmacomultiomics for Precision Medicine in Diabetes: A Comprehensive Review.Biomedicines · 2025Review
- Exploring biomarkers and molecular mechanisms of Type 2 diabetes mellitus promotes colorectal cancer progression based on transcriptomics.Scientific reports · 2025Article
- Exploring histone deacetylases in type 2 diabetes mellitus: pathophysiological insights and therapeutic avenues.Clinical epigenetics · 2024Review
- Histone deacetylase 7: a signalling hub controlling development, inflammation, metabolism and disease.The FEBS journal · 2023Review
- Down-regulation of histone deacetylase 7 reduces biological activities of retinal microvascular endothelial cells under high glucose condition and related mechanism.International journal of ophthalmology · 2023Article
- Pharmacological inhibitors of β-cell dysfunction and death as therapeutics for diabetes.Frontiers in endocrinology · 2023Review
- Pharmacoepigenetics in type 2 diabetes: is it clinically relevant?Diabetologia · 2022Article
- Epigenetics of type 2 diabetes mellitus and weight change - a tool for precision medicine?Nature reviews. Endocrinology · 2022Review
- Epigenetic modifications in pancreas development, diabetes, and therapeutics.Medicinal research reviews · 2022Review
- Review
- Post-GWAS functional studies reveal an RA-associated CD40-induced NF-kB signal transduction and transcriptional regulation network targeted by class II HDAC inhibitors.Human molecular genetics · 2021Article
- Epigenetics, microRNA and Metabolic Syndrome: A Comprehensive Review.International journal of molecular sciences · 2021Review
- Maternal obesity as a risk factor for developing diabetes in offspring: An epigenetic point of view.World journal of diabetes · 2021Review
- Epigenetic Regulation of PDX-1 in Type 2 Diabetes Mellitus.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Review
- Epigenetics in β-cell adaptation and type 2 diabetes.Current opinion in pharmacology · 2020Review
- Understanding Dietary Intervention-Mediated Epigenetic Modifications in Metabolic Diseases.Frontiers in genetics · 2020Review
- Circadian Genes as Therapeutic Targets in Pancreatic Cancer.Frontiers in endocrinology · 2020Review
- The challenge of correctly reporting hormones content and secretion in isolated human islets.Molecular metabolism · 2019Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
aimsIt has in recent years been established that epigenetic changes contribute to β-cell dysfunction and type 2 diabetes (T2D). For example, we have showed that the expression of histone deacetylase 7 (HDAC7) is increased in pancreatic islets of individuals with T2D and that increased levels of Hdac7 in β-cells impairs insulin secretion. The HDAC inhibitor MC1568 rescued this secretory impairment, suggesting that inhibitors specific for HDAC7 may be useful clinically in the treatment of T2D. The aim of the current study was to further explore HDAC7 as a novel therapeutic target in T2D.
methodsHdac7 was overexpressed in clonal β-cells followed by the analysis of insulin secretion, mitochondrial function, as well as cell number and apoptosis in the presence or absence of MC1568. Furthermore, the effect of MC1568 on insulin secretion in human pancreatic islets from non-diabetic donors and donors with T2D was also studied.
resultsOverexpression of Hdac7 in clonal β-cells significantly reduced insulin secretion, mitochondrial respiration, and ATP content, while it increased apoptosis. These impairments were all rescued by treatment with MC1568. The inhibitor also increased glucose-stimulated insulin secretion in islets from donors with T2D, while having no effect on islets from non-diabetic donors.
conclusionsHDAC7 inhibition protects β-cells from mitochondrial dysfunction and apoptosis, and increases glucose-stimulated insulin secretion in islets from human T2D donors. Our study supports specific HDAC7 inhibitors as novel options in the treatment of T2D.
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