ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2020
Sirt6-Mediated Endothelial-to-Mesenchymal Transition Contributes Toward Diabetic Cardiomyopathy via the Notch1 Signaling Pathway.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Lipophagy: A key regulator in oxidative stress and metabolic disorders.Genes & diseases · 2026Review
- Inhibitory Effect of Sirtuin6 on EndMT by Regulating Oxidative Stress and Autophagy in Coxsackievirus B3-Induced Cardiac Endothelial Cells.Immunity, inflammation and disease · 2025Article
- Metabolic and Immune Crosstalk in Cardiovascular Disease.Circulation research · 2025Review
- SIRT1: The first key to unlocking the mystery of cardiovascular diseases.Frontiers in pharmacology · 2025Review
- The role of nonmyocardial cells in the development of diabetic cardiomyopathy and the protective effects of FGF21: a current understanding.Cell communication and signaling : CCS · 2024Review
- Ferroptosis in diabetic cardiomyopathy: Advances in cardiac fibroblast-cardiomyocyte interactions.Heliyon · 2024Review
- Expression and significance of SIRT6 in human peritoneal dialysis effluents and peritoneal mesothelial cells.International urology and nephrology · 2024Article
- Exosomes derived from adipose tissue-derived stem cells alleviated HCell biology and toxicology · 2024Article
- Hsa_circ_0081065 exacerbates IH-induced EndMT via regulating miR-665/HIF-1α signal axis and HIF-1α nuclear translocation.Scientific reports · 2024Article
- Experimental Models to Study Endothelial to Mesenchymal Transition in Myocardial Fibrosis and Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- Cellular interplay between cardiomyocytes and non-myocytes in diabetic cardiomyopathy.Cardiovascular research · 2023Review
- Endothelial-to-Mesenchymal Transition: Potential Target of Doxorubicin-Induced Cardiotoxicity.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2023Review
- BASP1 promotes high glucose-induced endothelial apoptosis in diabetes via activation of EGFR signaling.Journal of diabetes investigation · 2023Article
- The role of mammalian Sirtuin 6 in cardiovascular diseases and diabetes mellitus.Frontiers in physiology · 2023Review
- Mitochondrial Sirtuins in Chronic Degenerative Diseases: New Metabolic Targets in Colorectal Cancer.International journal of molecular sciences · 2022Review
- Fibroblast-specific activation of Rnd3 protects against cardiac remodeling in diabetic cardiomyopathy via suppression of Notch and TGF-β signaling.Theranostics · 2022Article
- Ochratoxin A-Induced Nephrotoxicity: Up-to-Date Evidence.International journal of molecular sciences · 2021Review
- Endothelial-to-mesenchymal transition in systemic sclerosis.Clinical and experimental immunology · 2021Review
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEndothelial-to-mesenchymal transition (EndMT) is an important source of myofibroblasts that directly affects cardiac function in diabetic cardiomyopathy (DCM) via an unknown underlying mechanism. Sirt6 is a member of the Sirtuin family of NAD(+)-dependent enzymes that plays an important role in glucose and fatty acid metabolism. In this study, we investigated whether Sirt6 participates in EndMT during the development of T2DM and the possible underlying regulatory mechanisms.
methodsEndothelium-specific Sirt6 knockout (Sirt6-KO
resultsSirt6 expression is significantly downregulated in CMECs treated with HG+PA. Additionally, Sirt6-KO
conclusionThis study is the first to demonstrate that Sirt6 participates in EndMT via the Notch1 signaling pathway in CMECs stimulated with HG+PA. Therefore, the findings of this study suggest that Sirt6 could provide a potential treatment strategy for DCM.
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