ArticleAmerican journal of translational research2019
MiR-424 is over-expressed and attenuates ischemia-reperfusion kidney injury via p53 and death receptor 6 pathway.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- The molecular mechanisms and therapeutic potential of p53 in kidney injury repair: a perspective on the p53alpha/delta133p53alpha signaling axis.Renal failure · 2025Review
- DR6 Augments Colorectal Cancer Cell Growth, Invasion, and Stemness by Activating AKT/NF-κB Pathway.Biochemical genetics · 2025Article
- MicroRNAs as Biomarkers and Therapeutic Targets for Acute Kidney Injury.Diagnostics (Basel, Switzerland) · 2023Review
- MicroRNA-based engineering of mesenchymal stem cell extracellular vesicles for treatment of retinal ischemic disorders: Engineered extracellular vesiclesand retinal ischemia.Acta biomaterialia · 2023Article
- circ-AKT3 aggravates renal ischaemia-reperfusion injury via regulating miR-144-5p /Wnt/β-catenin pathway and oxidative stress.Journal of cellular and molecular medicine · 2022Article
- Antagonist targeting miR‑106b‑5p attenuates acute renal injury by regulating renal function, apoptosis and autophagy via the upregulation of TCF4.International journal of molecular medicine · 2021Article
- miRNA-182/Deptor/mTOR axis regulates autophagy to reduce intestinal ischaemia/reperfusion injury.Journal of cellular and molecular medicine · 2020Article
- Immunomodulatory and Regenerative Effects of Mesenchymal Stem Cell-Derived Extracellular Vesicles in Renal Diseases.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIschemic reperfusion injury of kidney is major cause for renal failure, however the involved pathogenesis remains unclear creating an void for its effective treatment. Here we studied involvement of microRNA-424 in renal injury.
methodsFor the study, p53 or HIF-1α mice were used, ischemic renal injury was induced using clamping of renal pedicles bilateraly. Proximal kidney tubular cells were used for
resultsWe discovered that, miR-424 was over-expressed in ischemic renal injury mice and in hypoxia exposed renal cells. In cells, miR-424 suppressed the expression levels of death receptor 6 (DR6) and halted the apoptosis mediated by hypoxia. Blocking of miR-424 halted the inhibition of DR6 and caused apoptosis and activation of caspase. In mice, miR-424 mimic inhibited expression of DR6 and attenuated ischemic renal injury. We established that, up-regulation of miR-424 in ischemic reperfusion injury was p53 dependent, also inhibition of p53 caused repression of miR-424 levels in hypoxia induced cells
conclusionThe study confirmed p53/miR-424/DR6 as a protective cascade during ischemic-reperfusion injury.
Indexed as
Identifiers
31105811PMC6511784W2996468037What OpenQuestion holds
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.