ArticleJournal of cellular and molecular medicine2026
HIF1α Attenuated the Lung Ischemia-Reperfusion Injury by Activating the miR-485/Notch1 Signalling.
Article in Journal of cellular and molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- Article
- The Simultaneous Prevention of Multiple Diseases: A "One Ring to Rule Them All" Framework for Redox-Driven Health and Longevity.Nutrients · 2026Review
- HIF1α Attenuated the Lung Ischemia-Reperfusion Injury by Activating the miR-485/Notch1 Signalling.Journal of cellular and molecular medicine · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Lung ischemia-reperfusion (I/R) injury is a common complication following lung transplantation and cardiac surgery. This study aimed to investigate the role and underlying mechanisms involving Neurogenic locus notch homologue protein 1 (Notch1) signalling and microRNA-485 (miR-485) of hypoxia-inducible factor 1-alpha (HIF1α) in protecting pulmonary microvascular endothelial cells (PMVECs) against I/R-induced injury. We found that overexpression of HIF1α significantly increased cell viability and decreased apoptosis in hypoxia/reoxygenation (H/R)-treated PMVECs, while knockdown or inhibition of HIF1α had the opposite effects. Moreover, HIF1α overexpression activated the Notch1 signalling pathway by upregulating Hes1 mRNA expression and Hes1 promoter activity. Conversely, HIF1α knockdown or inhibition inhibited Notch1 signalling. Furthermore, HIF1α overexpression alleviated H/R-induced mitophagy and mitochondrial dysfunction. On the other hand, HIF1α knockdown or inhibition aggravated mitophagy and mitochondrial dysfunction. We also found that HIF1α transcriptionally activated the expression of miR-485. Overexpression of miR-485 reversed the detrimental effects of HIF1α knockdown or inhibition on cell viability, apoptosis, Hes1 expression and mitophagy levels in H/R-treated PMVECs. Additionally, we identified NUMB endocytic adaptor protein (Numb) mRNA as a direct target of miR-485, and miR-485 overexpression suppressed Numb expression in PMVECs. In conclusion, these results suggest that targeting the HIF1α-miR-485-Numb axis may be a potential therapeutic strategy for attenuating lung I/R injury.
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Registered trials
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