ArticleFrontiers in immunology2022
Canagliflozin reverses Th1/Th2 imbalance and promotes podocyte autophagy in rats with membranous nephropathy.
Article in Frontiers in immunology, 2022. 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, 23 citations in OpenAlex.
- More than Glucose Elimination: Additional Benefits of SGLT2 Inhibitors in Glomerular Diseases.Drugs · 2026Review
- Programmed Cell Death: A Key Mechanism of Traditional Chinese Medicine in the Treatment of Membranous Nephropathy.Drug design, development and therapy · 2026Review
- Mechanism Study on the Regulation of Th1/Th2 in the Treatment of Idiopathic Membranous Nephropathy by Shengyang Yiwei Decoction.Combinatorial chemistry & high throughput screening · 2026Article
- Autophagy in the Pathogenesis of Membranous Nephropathy.Kidney medicine · 2025Review
- Mechanisms and Therapeutic Perspectives of Podocyte Aging in Podocytopathies.International journal of molecular sciences · 2025Review
- Targeting autophagy in autoimmune glomerular diseases.Journal of nephrology · 2025Review
- Potential Role of SGLT-2 Inhibitors in Improving Allograft Function and Reducing Rejection in Kidney Transplantation.Clinical transplantation · 2025Review
- SGLT2 Inhibitors in Glomerulonephritis: Beyond Nephroprotection?Journal of clinical medicine · 2025Review
- Impact of immune cell metabolism on membranous nephropathy and prospective therapy.Communications biology · 2025Review
- The alleviative effects of canagliflozin on imiquimod-induced mouse model of psoriasis-like inflammation.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- SGLT2 inhibitors in autoimmune diseases: emerging therapeutic potential and clinical challenges.Frontiers in immunology · 2025Review
- Unveiling the podocyte-protective effect of sodium-glucose cotransporter-2 inhibitors.Kidney research and clinical practice · 2025Article
- Intradermal delivery of SARS-CoV-2 RBD3-Fc mRNA vaccines via a needle-free injection system induces robust immune responses in rats.Frontiers in immunology · 2025Article
- The immunosuppressive mechanisms induced by sepsis and the corresponding treatment strategies.Frontiers in immunology · 2025Review
- Progress of SGLT2 inhibitors in the treatment of common immune-related nephropathies.International urology and nephrology · 2024Review
- mTOR and SGLT-2 Inhibitors: Their Synergistic Effect on Age-Related Processes.International journal of molecular sciences · 2024Review
- Sodium-Glucose Co-Transporter 2 Inhibitors: Mechanism of Action and Efficacy in Non-Diabetic Kidney Disease from Bench to Bed-Side.Journal of clinical medicine · 2024Review
- Pharmacological targets of SGLT2 inhibitors on IgA nephropathy and membranous nephropathy: a mendelian randomization study.Frontiers in pharmacology · 2024Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic membranous nephropathy is the main cause of chronic kidney disease (CKD). Studies have shown sodium-glucose co-transporter 2 (SGLT2) inhibitors significantly delay renal outcomes in patients with CKD, but the exact mechanism remains unknown. In this study, we investigated the mechanism by which the SGLT2 inhibitor canagliflozin attenuates podocyte injury by reversing the imbalance in Helper T cell 1 (Th1)/Helper T cell 2 (Th2) in peripheral blood of rats with membranous nephropathy (MN). MN rats were gavaged with canagliflozin (10 mg/kg/d) and losartan (10 mg/kg/d), respectively, for eight weeks. Compared with the MN group, the urinary ratio of total protein and the creatinine levels of the canagliflozin group decreased significantly. Canagliflozin improved the glomerulus pathological damage, increased the expression levels of podocyte marker proteins. The protective effect of canagliflozin on kidneys was more obvious than that of losartan. Treatment with canagliflozin increased the proportion of Th1 cells by 2.3 times, decreased the proportion of Th2 cells by 68.5%, and significantly restrained the synthesis of immunoglobulin G1 in B-cells and glomerulus subepithelial immune complex deposition. Co-culture of B-cells derived from MN rats with podocytes triggered the activation of phosphorylation of mTOR and ULK1 of podocytes, inhibited podocyte autophagy and resulted in podocyte injury. B-cells derived from canagliflozin treatment rats reversed these effects above. In conclusion, canagliflozin exerts a protective effect on kidneys by reversing the imbalance in Th1/Th2 cells in MN rats and restoring the autophagy of podocytes inhibited by the abnormal immunoglobulin G secretion from B-cells.
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