Article3 Biotech2021
Rapamycin inhibits LOC102553434-mediated pyroptosis to improve lung injury induced by limb ischemia-reperfusion.
Article in 3 Biotech, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 18 citations in OpenAlex.
- Fraxinellone mitigates acute lung injury by targeting HIF-1α to suppress pyroptosis and inflammation.Frontiers in immunology · 2026Article
- Article
- Bone marrow mesenchymal stem cell-derived exosomes miR-202-5p inhibited pyroptosis to alleviate lung ischemic-reperfusion injury by targeting CMPK2.The Kaohsiung journal of medical sciences · 2023Article
- MMP2 and MMP9 contribute to lung ischemia-reperfusion injury via promoting pyroptosis in mice.BMC pulmonary medicine · 2022Article
- A Novel Risk Model Identified Based on Pyroptosis-Related lncRNA Predicts Overall Survival and Associates With the Immune Landscape of GC Patients.Frontiers in genetics · 2022Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Limb ischemia reperfusion (I/R) triggers local or systemic injury, and whether the process is mediated by pyroptosis remains unclear, we aimed to explore whether pyroptosis was involved in the process of rapamycin alleviating lung injury induced by I/R and investigate the molecular mechanisms. The histopathology of lung injury induced by I/R was confirmed by hematoxylin-eosin (HE) staining, and malondialdehyde (MDA), superoxide dismutase (SOD), and the expression of pyroptosis related molecules were detected. RNA sequencing was used to mine key long non-coding RNAs (lncRNAs). The model of lipopolysaccharide (LPS)-induced L2 cell damage was also used to explore the effect and mechanism of rapamycin on lncRNA. Rapamycin treatment alleviated I/R-induced lung histopathologically injury and increased the concentration of MDA while decreased activity of SOD and expression of NLRP3, Caspase-1, interleukin-1β (IL-1β), and IL-18 in rat. A total of 63 differentially expressed lncRNAs (DElncRNAs) were identified from IR + Rap group compared with IR group, and these DElncRNAs were mainly involved in cell adhesion molecules (CAMs) and endocytosis pathway. The lncRNA LOC102553434 and its target gene MMP9 were most significantly up-regulated in I/R-injured rat. In vitro experiments showed that LPS induction caused a significant increase in LOC102553434, MMP9, IL-1β, and IL-18 in L2 cells, but rapamycin treatment significantly reversed the effects. After interfering with the expression of LOC102553434 in the LPS-injured cells pretreated with rapamycin, cell proliferation significantly increased, and the expression of MMP, NLRP3 and caspase-1 were significantly decreased. Rapamycin protects the lung from limb I/R injury by regulating LOC102553434 expression and inhibiting pyroptosis pathway. LOC102553434 plays a role in promoting pyroptosis and thus provides a target for clinical treatment of I/R-induced lung injury. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13205-021-02708-9.
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