ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2023
SGLT2 inhibitors prevent LPS-induced M1 macrophage polarization and alleviate inflammatory bowel disease by downregulating NHE1 expression.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
- NHE1 in Gastrointestinal Inflammation and Cancer: A Double-Edged Regulator.Digestive diseases and sciences · 2026Review
- Ex Vivo Human Colonic Explants Identify Metabolic Alterations and Cytokine Dysregulation in Ulcerative Colitis: A Pilot Study.Digestive diseases and sciences · 2026Article
- More than Glucose Elimination: Additional Benefits of SGLT2 Inhibitors in Glomerular Diseases.Drugs · 2026Review
- Metabolic Disorders and Inflammatory Bowel Diseases: Unraveling Shared Pathways and Clinical Interactions.Metabolites · 2026Review
- Targeting Skeletal Muscle in Duchenne Muscular Dystrophy: Integrating in Silico and Experimental Approaches to Sodium-Glucose Cotransporter-2 Inhibition.The American journal of pathology · 2026Article
- Sodium-glucose cotransporter-2 inhibitors and sepsis: a story with two tails or with one tail?Inflammopharmacology · 2026Review
- GBVAM as a Novel NHE1 Inhibitor Alleviates Doxorubicin-Induced Cardiotoxicity via PI3K/Akt/mTOR Pathway.Drug design, development and therapy · 2026Article
- Research progress on the molecular mechanisms of chlorogenic acid's pharmacological effects and its advanced drug delivery systems.Frontiers in pharmacology · 2026Review
- Inflammatory bowel disease and renal disorders: from clinical associations to shared mechanisms and management strategies.Frontiers in immunology · 2026Review
- NHE1 in macrophages promotes octanal/Olfr2-induced atherosclerosis via calcium-dependent ROS and NLRP3 inflammasome activation.Scientific reports · 2025Article
- Comparative risks of inflammatory bowel disease in patients with type 2 diabetes mellitus treated with SGLT-2 inhibitors versus DPP-4 inhibitors: a real-world nationwide cohort study.International journal of clinical pharmacy · 2025Article
- A Human Engineered Heart Tissue-Derived Lipotoxic Diabetic Cardiomyopathy Model Revealed Early Benefits of Empagliflozin.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Novel immune cross-talk between inflammatory bowel disease and IgA nephropathy.Renal failure · 2024Article
- Empagliflozin prevents heart failure through inhibition of the NHE1-NO pathway, independent of SGLT2.Basic research in cardiology · 2024Article
- Systemic and organ-specific anti-inflammatory effects of sodium-glucose cotransporter-2 inhibitors.Trends in endocrinology and metabolism: TEM · 2024Review
- Targeting Macrophages: Therapeutic Approaches in Diabetic Kidney Disease.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundClassically activated M1 macrophages, characterized by aberrant glycolysis and secretion of inflammatory cytokines, play pivotal roles in inflammatory diseases, including inflammatory bowel disease (IBD). Recently, sodium-glucose co-transporter 2 (SGLT2) inhibitors were shown to suppress Na
methodsWe analyzed cellular responses to SGLT2 inhibitors using mouse bone marrow-derived macrophages and peritoneal macrophages treated with lipopolysaccharide (LPS). To induce IBD, we used a dextran sulfate sodium salt-induced colitis mouse model.
resultsWe observed that NHE1 and NCX1 were overexpressed in LPS-treated macrophages, leading to M1 macrophage polarization. Mechanistically, NHE1 and NCX1-mediated Ca
conclusionsNHE1 promotes M1 macrophage polarization and SGLT2 inhibitors are a novel strategy to treat M1 macrophage-mediated inflammatory diseases, including IBD.
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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.