ArticleThe American journal of pathology2013
Excess podocyte semaphorin-3A leads to glomerular disease involving plexinA1-nephrin interaction.
Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- The role of the vascular niche in regulating kidney tubulointerstitial fibrosis.Kidney international · 2026Review
- Revisiting nephrin signaling and its specialized effects on the uniquely adaptable podocyte.The Biochemical journal · 2025Review
- Central role of podocytes in mediating cellular cross talk in glomerular health and disease.American journal of physiology. Renal physiology · 2024Review
- 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
- Rho-GTPase Activating Protein myosin MYO9A identified as a novel candidate gene for monogenic focal segmental glomerulosclerosis.Kidney international · 2021Article
- Semaphorin3A-Inhibitor Ameliorates Doxorubicin-Induced Podocyte Injury.International journal of molecular sciences · 2020Article
- Inhibitory effects of Semaphorin 3F as an alternative candidate to anti-VEGF monoclonal antibody on angiogenesis.In vitro cellular & developmental biology. Animal · 2019Article
- Inhibition of semaphorin-3a suppresses lipopolysaccharide-induced acute kidney injury.Journal of molecular medicine (Berlin, Germany) · 2018Article
- Nephrin Signaling in the Podocyte: An Updated View of Signal Regulation at the Slit Diaphragm and Beyond.Frontiers in endocrinology · 2018Review
- Podocyte Shape Regulation by Semaphorin 3A and MICAL-1.Methods in molecular biology (Clifton, N.J.) · 2017Article
- SLIT2/ROBO2 signaling pathway inhibits nonmuscle myosin IIA activity and destabilizes kidney podocyte adhesion.JCI insight · 2016Article
- FAT1 mutations cause a glomerulotubular nephropathy.Nature communications · 2016Article
- Vascular Growth Factors and Glomerular Disease.Annual review of physiology · 2016Review
- Role of Neuropilin-1 in Diabetic Nephropathy.Journal of clinical medicine · 2015Review
- Semaphorin3a promotes advanced diabetic nephropathy.Diabetes · 2015Article
- Podocyte-specific VEGF-a gain of function induces nodular glomerulosclerosis in eNOS null mice.Journal of the American Society of Nephrology : JASN · 2014Article
- Semaphorin3a signaling, podocyte shape, and glomerular disease.Pediatric nephrology (Berlin, Germany) · 2014Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Semaphorin-3A (Sema3a), a guidance protein secreted by podocytes, is essential for normal kidney patterning and glomerular filtration barrier development. Here, we report that podocyte-specific Sema3a gain-of-function in adult mice leads to proteinuric glomerular disease involving the three layers of the glomerular filtration barrier. Reversibility of the glomerular phenotype upon removal of the transgene induction provided proof-of-principle of the cause-and-effect relationship between podocyte Sema3a excess and glomerular disease. Mechanistically, excess Sema3a induces dysregulation of nephrin, matrix metalloproteinase 9, and αvβ3 integrin in vivo. Sema3a cell-autonomously disrupts podocyte shape. We identified a novel direct interaction between the Sema3a signaling receptor plexinA1 and nephrin, linking extracellular Sema3a signals to the slit-diaphragm signaling complex. We conclude that Sema3a functions as an extracellular negative regulator of the structure and function of the glomerular filtration barrier in the adult kidney. Our findings demonstrate a crosstalk between Sema3a and nephrin signaling pathways that is functionally relevant both in vivo and in vitro.
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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.