ArticleScientific reports2016
p53 activates miR-192-5p to mediate vancomycin induced AKI.
Article in Scientific reports, 2016. 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, 52 citations in OpenAlex.
- Endocytoscopic Classification Is Associated with Mucosal miR-192-5p Downregulation and CXCL2 Expression in Ulcerative Colitis: An Exploratory Study.Diagnostics (Basel, Switzerland) · 2026Article
- Beyond Junk DNA: Emerging Roles of Non-Coding RNAs in Cancer and Therapeutic Innovation.Biomolecules · 2026Review
- 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
- MicroRNA dysregulation in myelodysplastic syndromes: implications for diagnosis, prognosis, and therapeutic response.Frontiers in oncology · 2024Review
- Article
- Knockdown of deleterious miRNA in progenitor cell-derived small extracellular vesicles enhances tissue repair in myocardial infarction.Science advances · 2023Article
- A miRNA screening identifies miR-192-5p as associated with response to azacitidine and lenalidomide therapy in myelodysplastic syndromes.Clinical epigenetics · 2023Article
- HIPK2 as a Novel Regulator of Fibrosis.Cancers · 2023Review
- The Characterization and Differential Analysis of mAnimals : an open access journal from MDPI · 2023Article
- MicroRNA-192-5p downregulates Fat Mass and Obesity-associated Protein to aggravate renal ischemia/reperfusion injury.Renal failure · 2023Article
- Pifithrin-α ameliorates glycerol induced rhabdomyolysis and acute kidney injury by reducing p53 activation.Renal failure · 2022Article
- LncRNA ENSMUST_147219 mediates the progression of ischemic acute kidney injury by targeting the miR-221-5p/IRF6 axis.Apoptosis : an international journal on programmed cell death · 2022Article
- Expression and 7-day time course of circulating microRNAs in septic patients treated with nephrotoxic antibiotic agents.BMC nephrology · 2022Observational
- Preferential siRNA delivery to injured kidneys for combination treatment of acute kidney injury.Journal of controlled release : official journal of the Controlled Release Society · 2022Article
- Metabolic and Lipidomic Assessment of Kidney Cells Exposed to Nephrotoxic Vancomycin Dosages.International journal of molecular sciences · 2021Article
- MBD2 Mediates Septic AKI through Activation of PKCη/p38MAPK and the ERK1/2 Axis.Molecular therapy. Nucleic acids · 2021Article
- Knockdown of lncRNA ANRIL suppresses the production of inflammatory cytokines and mucin 5AC in nasal epithelial cells via the miR-15a-5p/JAK2 axis.Molecular medicine reports · 2021Article
- Emerging Role of MiR-192-5p in Human Diseases.Frontiers in pharmacology · 2021Review
- Circulating Extracellular Vesicles Carry Immune Regulatory miRNAs and Regulate Vaccine Efficacy and Local Inflammatory Response After Vaccination.Frontiers in immunology · 2021Review
- P53/miR-154 Pathway Regulates the Epithelial-Mesenchymal Transition in Glioblastoma Multiforme Cells by Targeting TCF12.Neuropsychiatric disease and treatment · 2021Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pathogenic role of p53 in AKI remains controversial and the underlying mechanism is unclear. Here, we tested whether the inhibition of p53 may ameliorate vancomycin (VAN) induced acute kidney injury (AKI). Mice with p53 knock out (p53-KO) were resistant to VAN induced AKI, indicated by the analysis of renal function, histology, and apoptosis. Mechanistically, AKI was associated with the upregulation of several known p53 target genes, including Bax and p21, and this association was attenuated in p53-KO mice. Furthermore, the expression of miR-192-5p was significantly decreased in the p53-KO kidney tissues. In human renal tubular epithelial cell line (HK-2), VAN induced p53 accumulation and miR-192-5p expression. Both apoptosis of HK-2 cells and expression of miR-192-5p were also suppressed by pifithrin-α. Anti-miR-192-5p significantly blocked VAN-induced apoptosis and caspase activity in HK-2 cells. Consistently, in vivo inhibition of miR-192-5p also suppressed VAN induced AKI. Thus, we provided clinical and genetic evidence that p53 was associated with the development of VAN induced AKI through upregulation of miR-192-5p.
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