ArticleInternational journal of molecular sciences2018
The Role of Trio, a Rho Guanine Nucleotide Exchange Factor, in Glomerular Podocytes.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Trans-ancestry GWAS identifies 59 loci and improves risk prediction and fine-mapping for kidney stone disease.Nature communications · 2025Pooled it
- Bevacizumab-induced hypertension and proteinuria: a genome-wide study of more than 1000 patients.British journal of cancer · 2022Trial
- Serum RAC1 as a potential biomarker in the early stages of diabetic kidney disease.Diabetology & metabolic syndrome · 2025Article
- CdGAP maintains podocyte function and modulates focal adhesions in a Src kinase-dependent manner.Scientific reports · 2022Article
- Epigenetics in the pathogenesis of diabetic nephropathy.Acta biochimica et biophysica Sinica · 2022Review
- Rho GTPases in kidney physiology and diseases.Small GTPases · 2022Article
- Ras-Related C3 Botulinum Toxin Substrate 1 Combining With the Mixed Lineage Kinase 3- Mitogen-Activated Protein Kinase 7- c-Jun N-Terminal Kinase Signaling Module Accelerates Diabetic Nephropathy.Frontiers in physiology · 2021Article
- Diverse Physiological Functions and Regulatory Mechanisms for Signal-Transducing Small GTPases.International journal of molecular sciences · 2020Article
- ARHGEF7 (Journal of the American Society of Nephrology : JASN · 2020Article
- Proteomics Analysis for Identification of Potential Cell Signaling Pathways and Protein Targets of Actions of Atractylodin and β-Eudesmol Against Cholangiocarcinoma.Asian Pacific journal of cancer prevention : APJCP · 2020Article
- Podocyte RhoGTPases: new therapeutic targets for nephrotic syndrome?F1000Research · 2019Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nephrotic syndrome is a kidney disease featured by heavy proteinuria. It is caused by injury to the specialized epithelial cells called "podocytes" within the filtration unit of the kidney, glomerulus. Previous studies showed that hyperactivation of the RhoGTPase, Rac1, in podocytes causes podocyte injury and glomerulosclerosis (accumulation of extracellular matrix in the glomerulus). However, the mechanism by which Rac1 is activated during podocyte injury is unknown. Trio is a guanine nucleotide exchange factor (GEF) known to activate Rac1. By RNA-sequencing, we found that Trio mRNA is abundantly expressed in cultured human podocytes. Trio mRNA was also significantly upregulated in humans with minimal change disease and focal segmental glomerulosclerosis, two representative causes of nephrotic syndrome. Reduced expression of Trio in cultured human podocytes decreased basal Rac1 activity, cell size, attachment to laminin, and motility. Furthermore, while the pro-fibrotic cytokine, transforming growth factor β1 increased Rac1 activity in control cells, it decreases Rac1 activity in cells with reduced Trio expression. This was likely due to simultaneous activation of the Rac1-GTPase activation protein, CdGAP. Thus, Trio is important in the basal functions of podocytes and may also contribute to glomerular pathology, such as sclerosis, via Rac1 activation.
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