ArticleScientific reports2021
Podocyte-specific Crb2 knockout mice develop focal segmental glomerulosclerosis.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- Disease-driven post-transcriptional alterations and alternative splicing in podocytes in focal segmental glomerulosclerosis.EMBO molecular medicine · 2026Article
- WTAP Deficiency Promotes Podocyte PANoptosis and FSGS via SPP1 Signaling.Circulation research · 2026Article
- Crumbs2 acts as a dynamic cellular sensor triggering stable podocyte cell-matrix anchorage.Biophysical journal · 2026Article
- CRB2 Facilitates Epithelial Ovarian Cancer Progression by Inducing Polarity Changes via Activation of the Wnt/PCP Signalling Pathway.Journal of cellular and molecular medicine · 2026Article
- A Novel CRB2 Mutation Associated With FSGS and ESRD in an Adult Patient.Case reports in nephrology · 2026Article
- Mechanisms and Therapeutic Perspectives of Podocyte Aging in Podocytopathies.International journal of molecular sciences · 2025Review
- Xanthohumol exerts protective function on adriamycin-induced podocyte injury.European journal of nutrition · 2025Article
- CRB2 depletion induces YAP signaling and disrupts mechanosensing in podocytes.American journal of physiology. Renal physiology · 2025Article
- The Pathogenesis of Nephrotic Syndrome: A Perspective from B Cells.Kidney diseases (Basel, Switzerland) · 2024Review
- The Protective Role of KANK1 in Podocyte Injury.International journal of molecular sciences · 2024Article
- Novel variants in CRB2 targeting the malfunction of slit diaphragm related to focal segmental glomerulosclerosis.Pediatric nephrology (Berlin, Germany) · 2024Article
- Recent Advances in Proteinuric Kidney Disease/Nephrotic Syndrome: Lessons from Knockout/Transgenic Mouse Models.Biomedicines · 2023Review
- Loss of surface transport is a main cellular pathomechanism of CRB2 variants causing podocytopathies.Life science alliance · 2023Article
- Association of Wilms tumor-1 protein in urinary exosomes with kidney injury: a population-based cross-sectional study.Frontiers in medicine · 2023Article
- Identification and characterization of Crumbs polarity complex proteins in Caenorhabditis elegans.The Journal of biological chemistry · 2022Article
- Anti-Apoptosis of Podocytes and Pro-Apoptosis of Mesangial Cells for Telmisartan in Alleviating Diabetic Kidney Injury.Frontiers in pharmacology · 2022Article
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Crb2 is a cell polarity-related type I transmembrane protein expressed in the apical membrane of podocytes. Knockdown of crb2 causes glomerular permeability defects in zebrafish, and its complete knockout causes embryonic lethality in mice. There are also reports of Crb2 mutations in patients with steroid-resistant nephrotic syndrome, although the precise mechanism is unclear. The present study demonstrated that podocyte-specific Crb2 knockout mice develop massive albuminuria and microhematuria 2-month after birth and focal segmental glomerulosclerosis and tubulointerstitial fibrosis with hemosiderin-laden macrophages at 6-month of age. Transmission and scanning electron microscopic studies demonstrated injury and foot process effacement of podocytes in 6-month aged podocyte-specific Crb2 knockout mice. The number of glomerular Wt1-positive cells and the expressions of Nphs2, Podxl, and Nphs1 were reduced in podocyte-specific Crb2 knockout mice compared to negative control mice. Human podocytes lacking CRB2 had significantly decreased F-actin positive area and were more susceptible to apoptosis than their wild-type counterparts. Overall, this study's results suggest that the specific deprivation of Crb2 in podocytes induces altered actin cytoskeleton reorganization associated with dysfunction and accelerated apoptosis of podocytes that ultimately cause focal segmental glomerulosclerosis.
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