ArticleDiabetes2017
Metallothionein Is Downstream of Nrf2 and Partially Mediates Sulforaphane Prevention of Diabetic Cardiomyopathy.
Article in Diabetes, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 2 of them syntheses that pooled it.
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Who cites it
114 citing papers in PubMed, 2 syntheses or guidelines pooled it, 191 citations in OpenAlex.
- What is the impact of ferroptosis on diabetic cardiomyopathy: a systematic review.Heart failure reviews · 2024Pooled it
- Sulforaphane ameliorates lipid profile in rodents: an updated systematic review and meta-analysis.Scientific reports · 2021Pooled it
- Restoring autophagy-apoptosis balance in diabetic cardiomyopathy via a biomimetic, ROS-responsive nanocarrier associated with Mst1 pathway modulation.Journal of nanobiotechnology · 2026Article
- Studies on Zinc Metabolism Related to Ischemia-reperfusion Injury: A Bibliometric and Visualized Analysis.Biological trace element research · 2026Review
- Transcriptional Heterogeneity of Cardiac Remodeling Between Type 1 and Type 2 Diabetes.Biomedicines · 2026Article
- Zinc Deficiency Aggravates High-Fat Diet-Induced Renal Injury by Regulating Oxidative Stress and Inflammation via the Nrf2/HO-1 Pathway.Biological trace element research · 2026Article
- Article
- Multi-omics atlas of ovarian cellular and molecular responses to diabetes.Molecular metabolism · 2026Article
- Right ventricular dysfunctions in type 1 diabetic mice: A longitudinal study.World journal of diabetes · 2025Article
- Emerging trends in cardiovascular diseases: the impact of ferroptosis and cuproptosis on cardiomyocyte death.Molecular and cellular biochemistry · 2025Review
- New insights into the role of metallothioneins in obesity and diabetes.International journal of obesity (2005) · 2025Review
- Novel impact of metal ion-induced cell death on diabetic cardiomyopathy pathogenesis and therapy.Apoptosis : an international journal on programmed cell death · 2025Review
- Therapeutic Approaches Targeting Ferroptosis in Cardiomyopathy.Cardiovascular drugs and therapy · 2025Review
- Aberrant activation of p53-TRIB3 axis contributes to diabetic myocardial insulin resistance and sulforaphane protection.Journal of advanced research · 2025Article
- Oral Sulforaphane Intervention Protects Against Diabetic Cardiomyopathy in db/db Mice: Focus on Cardiac Lipotoxicity and Substrate Metabolism.Antioxidants (Basel, Switzerland) · 2025Article
- Molecular Insights into Oxidative-Stress-Mediated Cardiomyopathy and Potential Therapeutic Strategies.Biomolecules · 2025Review
- New horizons for promising influences of sulforaphane in the management of metabolic syndrome: a mechanistic review.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Exercise and dietary interventions in the management of diabetic cardiomyopathy: mechanisms and implications.Cardiovascular diabetology · 2025Review
- Article
- Effects of Dapagliflozin on Myocardial Gene Expression in BTBR Mice with Type 2 Diabetes.Cardiovascular drugs and therapy · 2025Article
54 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have reported that sulforaphane (SFN) prevented diabetic cardiomyopathy in both type 1 and type 2 diabetes (T2DM) animal models via the upregulation of nuclear transcription factor erythroid 2-related factor 2 (Nrf2) and metallothionein (MT). In this study, we tested whether SFN protects the heart from T2DM directly through Nrf2, MT, or both. Using Nrf2-knockout (KO), MT-KO, and wild-type (WT) mice, T2DM was induced by feeding a high-fat diet for 3 months followed by a small dose of streptozotocin. Age-matched controls were given a normal diet. Both T2DM and control mice were then treated with or without SFN for 4 months by continually feeding a high-fat or normal diet. SFN prevented diabetes-induced cardiac dysfunction as well as diabetes-associated cardiac oxidative damage, inflammation, fibrosis, and hypertrophy, with increases in Nrf2 and MT expressions in the WT mice. Both Nrf2-KO and MT-KO diabetic mice exhibited greater cardiac damage than WT diabetic mice. SFN did not provide cardiac protection in Nrf2-KO mice, but partially or completely protected the heart from diabetes in MT-KO mice. SFN did not induce MT expression in Nrf2-KO mice, but stimulated Nrf2 function in MT-KO mice. These results suggest that Nrf2 plays the indispensable role for SFN cardiac protection from T2DM with significant induction of MT and other antioxidants. MT expression induced by SFN is Nrf2 dependent, but is not indispensable for SFN-induced cardiac protection from T2DM.
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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.