ArticleCellular & molecular biology letters2023
Overexpression of miR-92a attenuates kidney ischemia-reperfusion injury and improves kidney preservation by inhibiting MEK4/JNK1-related autophagy.
Article in Cellular & molecular biology letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Serum miR-381-3p: Diagnostic Role and Mechanisms in Liver Transplant Ischemia-reperfusion Injury.Journal of clinical and translational hepatology · 2026Article
- Apoptosis, Pyroptosis, and Necroptosis (PANoptosis) may be Present in Renal Ischemic Injury.Current medicinal chemistry · 2026Article
- Renal-targeted exosomes inhibiting miR-182-5p for treatment of renal ischemia-reperfusion injury.Bioengineering & translational medicine · 2026Article
- Review
- Nuclear receptor FXR inhibits ferroptosis to alleviate hepatic ischemia-reperfusion injury by targeting GPX4 in a mouse model.Journal of molecular histology · 2025Article
- miR-34a-5p modulation of polycystic ovary syndrome via targeting the NOTCH signaling pathway.Journal of ovarian research · 2025Article
- Enhancement of YTHDF2 plays a protective role in acute IRI models through downregulation of TUG1 expression.PloS one · 2025Article
- Protein swarm-based cause-effect analysis: effects of microRNAs on cooperation networks linking COVID-19 infections, atherosclerosis, and Alzheimer's disease.Frontiers in cardiovascular medicine · 2025Article
- MicroRNA-92a in Cardiovascular Disease: An Insufficiently Explored and Controversial Research Area.Cardiovascular drugs and therapy · 2024Article
- (Pro)renin receptor mediates tubular epithelial cell pyroptosis in diabetic kidney disease via DPP4-JNK pathway.Journal of translational medicine · 2024Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundKidney ischemia-reperfusion injury is inevitable in kidney transplantation, and is essential for primary graft dysfunction and delayed graft function. Our previous study has proved that miR-92a could ameliorate kidney ischemia-reperfusion injury, but the mechanism has not been studied.
methodsThis study conducted further research on the role of miR-92a in kidney ischemia-reperfusion injury and organ preservation. In vivo, mice models of bilateral kidney ischemia (30 min), cold preservation after ischemia (cold preservation time of 6, 12, and 24 h), and ischemia-reperfusion (reperfusion time of 24, 48, and 72 h) were established. Before or after modeling, the model mice were injected with miR-92a-agomir through the caudal vein. In vitro, the hypoxia-reoxygenation of HK-2 cells was used to simulate ischemia-reperfusion injury.
resultsKidney ischemia and ischemia-reperfusion significantly damaged kidney function, decreased the expression of miR-92a, and increased apoptosis and autophagy in kidneys. miR-92a agomir tail vein injection significantly increased the expression of miR-92a in kidneys, improved kidney function, and alleviated kidney injury, and the intervention before modeling achieved a better effect than after. Moreover, miR-92a agomir significantly reduced the apoptosis and autophagy in HK-2 cells induced by hypoxia, hypoxia-reoxygenation, and rapamycin, while miR-92a antagomir had opposite effects. Furthermore, mitogen-activated protein kinase, c-Jun NH (2) terminal kinase, caspase 3, Beclin 1, and microtubule-associated protein 1 light chain 3B were inhibited by overexpression of miR-92a both in vivo and in vitro, which in turn reduced apoptosis and autophagy.
conclusionsOur results prove that overexpression of miR-92a attenuated kidney ischemia-reperfusion injury and improved kidney preservation, and intervention before ischemia-reperfusion provides better protection than after.
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