ArticleNature communications2019
The tetraspanin CD9 controls migration and proliferation of parietal epithelial cells and glomerular disease progression.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- Genome-wide meta-analysis identifies new candidate genes for sickle cell disease nephropathy.Blood advances · 2023Pooled it
- Predictive value of CD44 in membranous nephropathy with focal segmental glomerular sclerosis lesions treated with calcineurin inhibitors.Renal failure · 2026Article
- Transcription factor 21 deletion from podocyte precursors as a model for congenital nephrotic syndrome.American journal of physiology. Renal physiology · 2026Article
- A population-scale atlas of blood and tissue in lupus nephritis.bioRxiv : the preprint server for biology · 2026Article
- Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Knock-down of the long isoform of the WNK1 kinase mitigates the anti-glomerular basement membrane glomerulonephritis in mice.Scientific reports · 2026Article
- Hypertension and age-related focal global glomerulosclerosis are associated with biomarkers for cellular senescence.Physiological reports · 2026Article
- Article
- Review
- Spatiotemporal interaction of immune and renal cells controls glomerular crescent formation in autoimmune kidney disease.Nature immunology · 2025Article
- The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025Review
- Article
- CD9 knockdown inhibits cell proliferation, migration, and invasion and augments apoptosis in tongue cancer cells through regulation of the EGFR signalling pathway.Molecular biology reports · 2025Article
- CD9-enriched extracellular vesicles from chemically reprogrammed basal progenitors of salivary glands mitigate salivary gland fibrosis.Bioactive materials · 2025Article
- CD9 expression in minimal change disease and focal segmental glomerulosclerosis.Clinical kidney journal · 2025Article
- Bowman's capsule rupture and its clinical significance in patients with anti-glomerular basement membrane disease.Frontiers in immunology · 2025Article
- ECHS1 as a Lipid Metabolism Biomarker for Pediatric Focal Segmental Glomerulosclerosis.PloS one · 2025Article
- Article
- CD9 Counteracts Liver Steatosis and Mediates GCGR Agonist Hepatic Effects.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Article
Corrections and comments
- Commented on by
- Commented on by
Authors and funding
33 authors at 11 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms driving the development of extracapillary lesions in focal segmental glomerulosclerosis (FSGS) and crescentic glomerulonephritis (CGN) remain poorly understood. A key question is how parietal epithelial cells (PECs) invade glomerular capillaries, thereby promoting injury and kidney failure. Here we show that expression of the tetraspanin CD9 increases markedly in PECs in mouse models of CGN and FSGS, and in kidneys from individuals diagnosed with these diseases. Cd9 gene targeting in PECs prevents glomerular damage in CGN and FSGS mouse models. Mechanistically, CD9 deficiency prevents the oriented migration of PECs into the glomerular tuft and their acquisition of CD44 and β1 integrin expression. These findings highlight a critical role for de novo expression of CD9 as a common pathogenic switch driving the PEC phenotype in CGN and FSGS, while offering a potential therapeutic avenue to treat these conditions.
Indexed as
Identifiers
What OpenQuestion holds
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.