ArticleJournal of the American Society of Nephrology : JASN2016
Podocyte p53 Limits the Severity of Experimental Alport Syndrome.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- GADD45A may be a potential biomarker associated with endoplasmic reticulum stress in focal segmental glomerulosclerosis.Biochemistry and biophysics reports · 2026Article
- Mechanisms and Therapeutic Perspectives of Podocyte Aging in Podocytopathies.International journal of molecular sciences · 2025Review
- Efficacy of Nrf2 activation in a proteinuric Alport syndrome mouse model.Life science alliance · 2025Article
- A novel mouse model for X-linked Alport syndrome induced by splicing mutation in the Col4a5 gene.Scientific reports · 2025Article
- Renal Phenotype Variations among Families with Autosomal Alport Syndrome: Potential Role of Modifier Genes.Kidney360 · 2025Article
- Role of the Innate Immune Response in Glomerular Disease Pathogenesis: Focus on Podocytes.Cells · 2024Review
- iPSC-derived type IV collagen α5-expressing kidney organoids model Alport syndrome.Communications biology · 2023Article
- Review
- Echinochrome A Prevents Diabetic Nephropathy by Inhibiting the PKC-Iota Pathway and Enhancing Renal Mitochondrial Function in db/db Mice.Marine drugs · 2023Article
- The role of discoidin domain receptor 2 in the renal dysfunction of alport syndrome mouse model.Renal failure · 2021Article
- Metformin ameliorates the severity of experimental Alport syndrome.Scientific reports · 2021Article
- Article
- The Use of High-Throughput Transcriptomics to Identify Pathways with Therapeutic Significance in Podocytes.International journal of molecular sciences · 2019Article
- Cancer driver mutations in endometriosis: Variations on the major theme of fibrogenesis.Reproductive medicine and biology · 2018Review
- lncRNA ZEB1-AS1 Was Suppressed by p53 for Renal Fibrosis in Diabetic Nephropathy.Molecular therapy. Nucleic acids · 2018Article
- Pathogenicity of a Human LamininJournal of the American Society of Nephrology : JASN · 2018Article
- Long-term treatment with EGFR inhibitor erlotinib attenuates renal inflammatory cytokines but not nephropathy in Alport syndrome mouse model.Clinical and experimental nephrology · 2017Article
- C-X-C Chemokine Receptor Type 4 Plays a Crucial Role in Mediating Oxidative Stress-Induced Podocyte Injury.Antioxidants & redox signaling · 2017Article
- Autophagy is involved in mouse kidney development and podocyte differentiation regulated by Notch signalling.Journal of cellular and molecular medicine · 2017Article
- p53 induces miR199a-3p to suppress SOCS7 for STAT3 activation and renal fibrosis in UUO.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alport syndrome (AS) is one of the most common types of inherited nephritis caused by mutation in one of the glomerular basement membrane components. AS is characterized by proteinuria at early stage of the disease and glomerular hyperplastic phenotype and renal fibrosis at late stage. Here, we show that global deficiency of tumor suppressor p53 significantly accelerated AS progression in X-linked AS mice and decreased the lifespan of these mice. p53 protein expression was detected in 21-week-old wild-type mice but not in age-matched AS mice. Expression of proinflammatory cytokines and profibrotic genes was higher in p53(+/-) AS mice than in p53(+/+) AS mice. In vitro experiments revealed that p53 modulates podocyte migration and positively regulates the expression of podocyte-specific genes. We established podocyte-specific p53 (pod-p53)-deficient AS mice, and determined that pod-p53 deficiency enhanced the AS-induced renal dysfunction, foot process effacement, and alteration of gene-expression pattern in glomeruli. These results reveal a protective role of p53 in the progression of AS and in maintaining glomerular homeostasis by modulating the hyperplastic phenotype of podocytes in AS.
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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.