ArticleScientific reports2017
Sodium-myoinositol cotransporter-1, SMIT1, mediates the production of reactive oxygen species induced by hyperglycemia in the heart.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.
- Genomic insights about the effect of sodium-glucose cotransporter 2 inhibitors: a systematic review.Frontiers in genetics · 2025Pooled it
- PlasmaMetabolomics : Official journal of the Metabolomic Society · 2026Article
- Sodium-myo-inositol cotransporter-1, SMIT1, promotes cardiac hypertrophy and fibrosis induced by pressure overload in mice.Cardiovascular research · 2026Article
- Sotagliflozin Enhances Left Ventricular Function and Myocardial Perfusion in Chronic Myocardial Ischemia Through Metabolic and Redox Remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Cardiac sodium-glucose co-transporter 1 (SGLT1) contributes to heart failure in a mouse model of diabetic cardiomyopathy.Basic research in cardiology · 2025Article
- Sodium-myoinositol cotransporter-1 downstream of m6A methyltransferase WTAP exerts a potential carcinogenicity in diffuse large B-cell lymphoma progression.Journal of translational medicine · 2025Article
- Comparison of the Effects of Sodium-Glucose Cotransporter 2 Inhibitors on Cardiac Fibroblast Properties.International journal of molecular sciences · 2025Article
- Identification of potential biomarkers of triton WR-1339 induced hyperlipidemia: NMR-based plasma metabolomics approach and gene expression analysis.Metabolomics : Official journal of the Metabolomic Society · 2025Article
- SGLT2 Inhibitors: From Structure-Effect Relationship to Pharmacological Response.International journal of molecular sciences · 2025Review
- Targeting Lactic Acid Modification in Ischemic Heart Diseases: Novel Therapeutics and Mechanism.Journal of cardiovascular translational research · 2025Review
- ApoE2 affects insulin signaling in the hippocampus and spatial cognition of aged mice in a sex-dependent manner.Cell communication and signaling : CCS · 2025Article
- Anti-inflammatory Therapies for Ischemic Heart Disease.Current cardiology reports · 2025Review
- Leveraging metabolism for better outcomes in heart failure.Cardiovascular research · 2024Review
- Sodium-Glucose Cotransporter 2 (SGLT2) Inhibitors: Guardians against Mitochondrial Dysfunction and Endoplasmic Reticulum Stress in Heart Diseases.ACS pharmacology & translational science · 2024Review
- SGLT1 contributes to glucose-mediated exacerbation of ischemia-reperfusion injury in ex vivo rat heart.Basic research in cardiology · 2024Article
- SGLT2 inhibitors protect against diabetic cardiomyopathy and atrial fibrillation through a CaMKII independent mechanism.bioRxiv : the preprint server for biology · 2024Article
- Acute Hyperglycemia-Induced Injury in Myocardial Infarction.International journal of molecular sciences · 2024Review
- Unsupervised clustering identified clinically relevant metabolic syndrome endotypes in UK and Taiwan Biobanks.iScience · 2024Article
- The SGLT2 inhibitor empagliflozin inhibits skeletal muscle fibrosis in naturally aging male mice through the AMPKα/MMP9/TGF-β1/Smad pathway.Biogerontology · 2024Article
- Role and molecular mechanisms of SGLT2 inhibitors in pathological cardiac remodeling (Review).Molecular medicine reports · 2024Review
Corrections and comments
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Authors and funding
18 authors at 5 institutions in 3 countries.
Funding
Abstract
Hyperglycemia (HG) stimulates the production of reactive oxygen species in the heart through activation of NADPH oxidase 2 (NOX2). This production is independent of glucose metabolism but requires sodium/glucose cotransporters (SGLT). Seven SGLT isoforms (SGLT1 to 6 and sodium-myoinositol cotransporter-1, SMIT1) are known, although their expression and function in the heart remain elusive. We investigated these 7 isoforms and found that only SGLT1 and SMIT1 were expressed in mouse, rat and human hearts. In cardiomyocytes, galactose (transported through SGLT1) did not activate NOX2. Accordingly, SGLT1 deficiency did not prevent HG-induced NOX2 activation, ruling it out in the cellular response to HG. In contrast, myo-inositol (transported through SMIT1) reproduced the toxic effects of HG. SMIT1 overexpression exacerbated glucotoxicity and sensitized cardiomyocytes to HG, whereas its deletion prevented HG-induced NOX2 activation. In conclusion, our results show that heart SMIT1 senses HG and triggers NOX2 activation. This could participate in the redox signaling in hyperglycemic heart and contribute to the pathophysiology of diabetic cardiomyopathy.
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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 Socratic graph.