ArticleJournal of molecular medicine (Berlin, Germany)2014
Urinary semaphorin 3A correlates with diabetic proteinuria and mediates diabetic nephropathy and associated inflammation in mice.
Article in Journal of molecular medicine (Berlin, Germany), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Role of Semaphorin 3A in Kidney Development and Diseases.Diagnostics (Basel, Switzerland) · 2023Review
- LncRNA TCF7 contributes to high glucose-induced damage in human podocytes by up-regulating SEMA3A via sponging miR-16-5p.Journal of diabetes investigation · 2023Article
- Low Urine Secretion of Semaphorin3A in Lupus Patients with Proteinuria.Inflammation · 2022Article
- The effects of voluntary complex and regular wheel running exercises on the levels of 8-oxoguanine DNA glycosylase, semaphorin 3B, H2O2, and apoptosis in the hippocampus of diabetic rats.Brain and behavior · 2021Article
- Glomerular Endothelial Cell Crosstalk With Podocytes in Diabetic Kidney Disease.Frontiers in medicine · 2021Review
- The Role of Semaphorins in Metabolic Disorders.International journal of molecular sciences · 2020Review
- Semaphorin3A-Inhibitor Ameliorates Doxorubicin-Induced Podocyte Injury.International journal of molecular sciences · 2020Article
- Recognizable type of pituitary, heart, kidney and skeletal dysplasia mostly caused byWorld journal of clinical cases · 2019Article
- Inhibition of semaphorin-3a suppresses lipopolysaccharide-induced acute kidney injury.Journal of molecular medicine (Berlin, Germany) · 2018Article
- Inducible overexpression of endothelial proNGF as a mouse model to study microvascular dysfunction.Biochimica et biophysica acta. Molecular basis of disease · 2018Article
- The level of urinary semaphorin3A is associated with disease activity in patients with minimal change nephrotic syndrome.International journal of nephrology and renovascular disease · 2017Article
- A novel podocyte gene, semaphorin 3G, protects glomerular podocyte from lipopolysaccharide-induced inflammation.Scientific reports · 2016Article
- Low-Dose IL-17 Therapy Prevents and Reverses Diabetic Nephropathy, Metabolic Syndrome, and Associated Organ Fibrosis.Journal of the American Society of Nephrology : JASN · 2016Article
- Deletion of UNC5B in Kidney Epithelium Exacerbates Diabetic Nephropathy in Mice.American journal of nephrology · 2015Article
- Semaphorin-3A is a repulsive but attractive renal guidance cue to therapy.Journal of molecular medicine (Berlin, Germany) · 2014Article
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8 authors.
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Abstract
Semaphorin 3A (sema3A) was recently identified as an early diagnostic biomarker of acute kidney injury. However, its role as a biomarker and/or mediator of chronic kidney disease (CKD) related to diabetic nephropathy is unknown. We examined the expression of sema3A in diabetic animal models and in humans and tested whether sema3A plays a pathogenic role in the development of diabetic nephropathy. The expression of sema3A was localized to podocytes and epithelial cells in distal tubules and collecting ducts in control animals, and its expression was increased following the induction of diabetes. Quantification of sema3A urinary excretion in three different diabetic mouse models showed that excretion was increased as early as 2 weeks after the induction of diabetes and increased over time, in conjunction with the development of nephropathy. Consistent with the mouse data, increased sema3A urinary excretion was detected in diabetic patients with albuminuria, particularly in those with macroalbuminuria. Genetic ablation of sema3A or pharmacological inhibition with a novel sema3A inhibitory peptide was protected against diabetes-induced albuminuria, kidney fibrosis, inflammation, oxidative stress, and renal dysfunction. We conclude that sema3A is both a biomarker and a mediator of diabetic kidney disease and could be a promising therapeutic target in diabetic nephropathy. Key messages Diabetes induced sema3A excretion in urine. Increased semaphorin 3A was associated with severity of albuminuria. Seme3A-mediated diabetes induced glomerulosclerosis. Peptide-based inhibition of semaphorin3A suppressed diabetic nephropathy.
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