ArticleJournal of the American Society of Nephrology : JASN2017
Suppressor of Cytokine Signaling-1 Peptidomimetic Limits Progression of Diabetic Nephropathy.
Article in Journal of the American Society of Nephrology : JASN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 53 citations in OpenAlex.
- Immunoregulatory and lipid presentation pathways are upregulated in human face transplant rejection.The Journal of clinical investigation · 2021Trial
- Acarbose Reduces Low-Grade Albuminuria Compared to Metformin in Chinese Patients with Newly Diagnosed Type 2 Diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Trial
- SOCS1-based therapeutic peptides improve liver disease and metabolic dysfunction in obesity and diabetes.Scientific reports · 2026Article
- SOCS1 Mimetic Peptide Enhances Empagliflozin Improvement on Kidney Damage in the Type 2 Diabetes Mouse Model BTBR ob/ob.International journal of molecular sciences · 2026Article
- Opposing functions of miR-155-5p and Socs1 drive vascular inflammation in diabetes-accelerated atherosclerosis.Cardiovascular diabetology · 2026Article
- The role of extracellular vesicles in kidney disease progression.Kidney research and clinical practice · 2026Article
- The Association of Diabetes and Atherosclerosis: Understanding the Molecular Mechanism of the Double Burden.Current medicinal chemistry · 2026Review
- Integrated bulk and single-cell transcriptomics identify RELB, S100A9, and SOCS1 as key autophagy-endoplasmic reticulum stress genes linking T2DM with MAFLD.Scientific reports · 2025Article
- Inflammation in glomerular diseases.Frontiers in immunology · 2025Review
- A mutual regulatory loop between miR-155 and SOCS1 influences renal inflammation and diabetic kidney disease.Molecular therapy. Nucleic acids · 2023Article
- Sitagliptin Mitigates Diabetic Nephropathy in a Rat Model of Streptozotocin-Induced Type 2 Diabetes: Possible Role of PTP1B/JAK-STAT Pathway.International journal of molecular sciences · 2023Article
- Structure-Activity Relationship Investigations of Novel Constrained Chimeric Peptidomimetics of SOCS3 Protein Targeting JAK2.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Activation of the NLRP3 inflammasome by RAC1 mediates a new mechanism in diabetic nephropathy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- Detrimental Effect of Cannabidiol on the Early Onset of Diabetic Nephropathy in Male Mice.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Review
- Suppressor of cytokine signaling-1 mimetic peptides attenuate lymphocyte activation in the MRL/lpr mouse autoimmune model.Scientific reports · 2021Article
- Toll-Like Receptors in Acute Kidney Injury.International journal of molecular sciences · 2021Review
- Tubular cell-derived exosomal miR-150-5p contributes to renal fibrosis following unilateral ischemia-reperfusion injury by activating fibroblastInternational journal of biological sciences · 2021Article
- Proteomimetics of Natural Regulators of JAK-STAT Pathway: Novel Therapeutic Perspectives.Frontiers in molecular biosciences · 2021Review
- Neurogenic tachykinin mechanisms in experimental nephritis of rats.Pflugers Archiv : European journal of physiology · 2020Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetes is the main cause of CKD and ESRD worldwide. Chronic activation of Janus kinase and signal transducer and activator of transcription (STAT) signaling contributes to diabetic nephropathy by inducing genes involved in leukocyte infiltration, cell proliferation, and extracellular matrix accumulation. This study examined whether a cell-permeable peptide mimicking the kinase-inhibitory region of suppressor of cytokine signaling-1 (SOCS1) regulatory protein protects against nephropathy by suppressing STAT-mediated cell responses to diabetic conditions. In a mouse model combining hyperglycemia and hypercholesterolemia (streptozotocin diabetic, apoE-deficient mice), renal STAT activation status correlated with the severity of nephropathy. Notably, compared with administration of vehicle or mutant inactive peptide, administration of the SOCS1 peptidomimetic at either early or advanced stages of diabetes ameliorated STAT activity and resulted in reduced serum creatinine level, albuminuria, and renal histologic changes (mesangial expansion, tubular injury, and fibrosis) over time. Mice treated with the SOCS1 peptidomimetic also exhibited reduced kidney leukocyte recruitment (T lymphocytes and classic M1 proinflammatory macrophages) and decreased expression levels of proinflammatory and profibrotic markers that were independent of glycemic and lipid changes. In vitro, internalized peptide suppressed STAT activation and target gene expression induced by inflammatory and hyperglycemic conditions, reduced migration and proliferation in mesangial and tubuloepithelial cells, and altered the expression of cytokine-induced macrophage polarization markers. In conclusion, our study identifies SOCS1 mimicking as a feasible therapeutic strategy to halt the onset and progression of renal inflammation and fibrosis in diabetic kidney disease.
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