ArticleJournal of the American Society of Nephrology : JASN2014
Targeted deletion of p53 in the proximal tubule prevents ischemic renal injury.
Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
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Who cites it
86 citing papers in PubMed, 117 citations in OpenAlex.
- Pregnane X receptor mitigates aristolochic acid-induced acute kidney injury via p53 ubiquitination.Renal failure · 2026Article
- Epitope-diverse autoantibodies induce neutrophil-epithelial niches driving kidney injury in ANCA-associated glomerulonephritis.The Journal of experimental medicine · 2026Article
- Involvement of c-Myc/WWP1/TRIM65 Axis in Renal Fibrosis.Biomolecules · 2026Article
- Exploring the Therapeutic Role of Pregnane X Receptor Activation in Acute Kidney Injury: Mechanisms and Clinical Implications.Current molecular medicine · 2026Review
- Small Interfering RNA (siRNA) for Cardiorenal Disease: Mechanistic Insights from Preclinical and Clinical Studies.Journal of cardiovascular translational research · 2025Review
- Early single session of hyperbaric oxygen therapy mitigates renal apoptosis in lipopolysaccharides-induced endotoxemia in rats.Kidney research and clinical practice · 2025Article
- Adding insult to injury: the spectrum of tubulointerstitial responses in acute kidney injury.The Journal of clinical investigation · 2025Review
- siRNA-mediated therapeutic approaches improve acute kidney injury and limit its worsening.Frontiers in pharmacology · 2025Review
- The crosstalk of Wnt/β-catenin signaling and p53 in acute kidney injury and chronic kidney disease.Kidney research and clinical practice · 2024Article
- Cell death induced by acute renal injury: a perspective on the contributions of accidental and programmed cell death.American journal of physiology. Renal physiology · 2024Review
- Targeting tumor suppressor p53 for organ fibrosis therapy.Cell death & disease · 2024Review
- Nanomedicine embraces the treatment and prevention of acute kidney injury to chronic kidney disease transition: evidence, challenges, and opportunities.Burns & trauma · 2024Review
- Aquaporin 1 is renoprotective in septic acute kidney injury by attenuating inflammation, apoptosis and fibrosis through inhibition of P53 expression.Frontiers in immunology · 2024Article
- Proximal TubularInternational journal of molecular sciences · 2023Article
- Pregnane X receptor activation alleviates renal fibrosis in mice via interacting with p53 and inhibiting the Wnt7a/β-catenin signaling.Acta pharmacologica Sinica · 2023Article
- Early Growth Response 1 Contributes to Renal IR Injury by Inducing Proximal Tubular Cell Apoptosis.International journal of molecular sciences · 2023Article
- Streptozotocin induces renal proximal tubular injury through p53 signaling activation.Scientific reports · 2023Article
- Echinochrome A Prevents Diabetic Nephropathy by Inhibiting the PKC-Iota Pathway and Enhancing Renal Mitochondrial Function in db/db Mice.Marine drugs · 2023Article
- A molecular network-based pharmacological study on the protective effect ofFrontiers in pharmacology · 2023Article
- Endotoxin induced acute kidney injury modulates expression of AQP1, P53 and P21 in rat kidney, heart, lung and small intestine.PloS one · 2023Article
26 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
The contribution of p53 to kidney dysfunction, inflammation, and tubular cell death, hallmark features of ischemic renal injury (IRI), remains undefined. Here, we studied the role of proximal tubule cell (PTC)-specific p53 activation on the short- and long-term consequences of renal ischemia/reperfusion injury in mice. After IRI, mice with PTC-specific deletion of p53 (p53 knockout [KO]) had diminished whole-kidney expression levels of p53 and its target genes, improved renal function, which was shown by decreased plasma levels of creatinine and BUN, and attenuated renal histologic damage, oxidative stress, and infiltration of neutrophils and macrophages compared with wild-type mice. Notably, necrotic cell death was attenuated in p53 KO ischemic kidneys as well as oxidant-injured p53-deficient primary PTCs and pifithrin-α-treated PTC lines. Reduced oxidative stress and diminished expression of PARP1 and Bax in p53 KO ischemic kidneys may account for the decreased necrosis. Apoptosis and expression of proapoptotic p53 targets, including Bid and Siva, were also significantly reduced, and cell cycle arrest at the G2/M phase was attenuated in p53 KO ischemic kidneys. Furthermore, IRI-induced activation of TGF-β and the long-term development of inflammation and interstitial fibrosis were significantly reduced in p53 KO mice. In conclusion, specific deletion of p53 in the PTC protects kidneys from functional and histologic deterioration after IRI by decreasing necrosis, apoptosis, and inflammation and modulates the long-term sequelae of IRI by preventing interstitial fibrogenesis.
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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.