ArticleCell proliferation2017
Rapamycin suppresses hypoxia/reoxygenation-induced islet injury by up-regulation of miR-21 via PI3K/Akt signalling pathway.
Article in Cell proliferation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Can miRNAs in MSCs-EVs Offer a Potential Treatment for Hypoxic-ischemic Encephalopathy?Stem cell reviews and reports · 2025Review
- Small RNA-Seq and real time rt-qPCR reveal islet miRNA released under stress conditions.Islets · 2024Article
- Crosstalk between MiRNAs/lncRNAs and PI3K/AKT signaling pathway in diabetes mellitus: Mechanistic and therapeutic perspectives.Non-coding RNA research · 2024Review
- Thioredoxin-interacting protein: a critical link between autophagy disorders and pancreatic β-cell dysfunction.Endocrine · 2020Article
- Amniotic Membrane Extract Protects Islets From Serum-Deprivation Induced Impairments and Improves Islet Transplantation Outcome.Frontiers in endocrinology · 2020Article
- miR-21 enhances the protective effect of loperamide on rat cardiomyocytes against hypoxia/reoxygenation, reactive oxygen species production and apoptosis via regulating Akap8 and Bard1 expression.Experimental and therapeutic medicine · 2019Article
- Effect of Platelet-rich Plasma on Implant Bone Defects in Rabbits Through the FAK/PI3K/AKT Signaling Pathway.Open life sciences · 2019Article
- Regulatory effect of immunosuppressive agents in mice with renal ischemia reperfusion injury.Experimental and therapeutic medicine · 2018Article
- Rapamycin-induced miR-21 promotes mitochondrial homeostasis and adaptation in mTORC1 activated cells.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesIncreasing evidences indicate that microRNAs may play a critical role in the regulation of hypoxia/reoxygenation (H/R) injury, and their expression is associated with mTORC activity. We propose that rapamycin modulates H/R-induced islets injury by regulating microRNA expression. MATERIALS AND
methodsWe investigated whether rapamycin treatment could alter the expression profile of miRNAs in islets. Furthermore, we assessed the islet apoptosis and function after H/R or syngeneic islet transplantation.
resultsWe found that rapamycin treatment significantly decreased H/R-induced islet apoptosis, and improved islet function in vivo and in vitro, and that miR-21 gene transcription is controlled by rapamycin. When the PI3k/Akt signalling pathways was blocked by wortmannin, the up-regulative effects of rapamycin on miR-21 expression were inhibited in vitro. Furthermore, our study clearly demonstrates that miR-21 is essential for the rapamycin-mediated protection islets against H/R injury. DISCUSSION: Our findings indicate that up-regulation of miR-21 function in islets by treatment with rapamycin or overexpression of the miR-21 could represent a potential new therapy for the treatment of H/R injury.
conclusionThe results of this study clearly suggest that rapamycin exerts its inhibitory effects on islets H/R injury by inducing miR-21 expression via PI3K/Akt.
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