ReviewCellular and molecular life sciences : CMLS2022
Emerging role of tumor suppressor p53 in acute and chronic kidney diseases.
Review in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- Pregnane X receptor mitigates aristolochic acid-induced acute kidney injury via p53 ubiquitination.Renal failure · 2026Article
- Empagliflozin, Linagliptin, and Metformin Differentially Affect Renal PI3K/Akt and MAPK/ERK Signaling Pathways inInternational journal of molecular sciences · 2026Article
- Apoptosis and Cell Cycle Dysregulation in AmpligoJournal of xenobiotics · 2026Article
- Targeting DNA Damage and Repair Pathways in Cerebral Ischemic Stroke: From Bench to Bedside.Translational stroke research · 2026Review
- UBE2M Identified by CRISPR Screening as a Key Regulator of Cisplatin-Induced Acute Kidney Injury via the p53 PathwayEndocrine, metabolic & immune disorders drug targets · 2026Article
- What new renal biomarkers tell us about renal physiology: Collection: physiology applied to ICU.Annals of intensive care · 2026Review
- Minichromosome maintenance 4 plays a key role in protecting against acute kidney injury by regulating tubular epithelial cells survival and regeneration.Journal of advanced research · 2026Article
- Exploring the Therapeutic Role of Pregnane X Receptor Activation in Acute Kidney Injury: Mechanisms and Clinical Implications.Current molecular medicine · 2026Review
- Immunolocalization of p53 and p21 in Kidneys Exposed to T-2 Mycotoxin.Current issues in molecular biology · 2025Article
- The molecular mechanisms and therapeutic potential of p53 in kidney injury repair: a perspective on the p53alpha/delta133p53alpha signaling axis.Renal failure · 2025Review
- Mesenchymal stem cells inhibit mitochondrial fission by upregulating armadillo repeat containing 1, ameliorating oxidative stress in renal fibrosis.Stem cell research & therapy · 2025Article
- The Impact of METTL3 on MDM2 Promotes Podocytes Injury During Diabetic Kidney Disease.Journal of cellular and molecular medicine · 2025Article
- A Novel Mechanism of the p53 Isoform Δ40p53α in Regulating Collagen III Expression in TGFβ1-Induced LX-2 Human Hepatic Stellate Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Gut microbiota-derived SCFAs and MetS-related nephropathy.Frontiers in nutrition · 2025Review
- Tumor hypoxia evidences the differential regulation of Mdm2-p53 axis by PTEN in tumor derived vs. normal endothelial cells.Scientific reports · 2024Article
- Podocyte Death in Diabetic Kidney Disease: Potential Molecular Mechanisms and Therapeutic Targets.International journal of molecular sciences · 2024Review
- Article
- Transcriptome Profiling ofMicroorganisms · 2023Article
- Emerging role and therapeutic implications of p53 in intervertebral disc degeneration.Cell death discovery · 2023Review
- Pregnane X receptor activation alleviates renal fibrosis in mice via interacting with p53 and inhibiting the Wnt7a/β-catenin signaling.Acta pharmacologica Sinica · 2023Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
p53 is a major regulator of cell cycle arrest, apoptosis, and senescence. While involvement of p53 in tumorigenesis is well established, recent studies implicate p53 in the initiation and progression of several renal diseases, which is the focus of this review. Ischemic-, aristolochic acid (AA) -, diabetic-, HIV-associated-, obstructive- and podocyte-induced nephropathies are accompanied by activation and/or elevated expression of p53. Studies utilizing chemical or renal-specific inhibition of p53 in mice confirm the pathogenic role of this transcription factor in acute kidney injury and chronic kidney disease. TGF-β1, NOX, ATM/ATR kinases, Cyclin G, HIPK, MDM2 and certain micro-RNAs are important determinants of renal p53 function in response to trauma. AA, cisplatin or TGF-β1-mediated ROS generation via NOXs promotes p53 phosphorylation and subsequent tubular dysfunction. p53-SMAD3 transcriptional cooperation downstream of TGF-β1 orchestrates induction of fibrotic factors, extracellular matrix accumulation and pathogenic renal cell communication. TGF-β1-induced micro-RNAs (such as mir-192) could facilitate p53 activation, leading to renal hypertrophy and matrix expansion in response to diabetic insults while AA-mediated mir-192 induction regulates p53 dependent epithelial G
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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.