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| Mechanistic Study on the Role of SNHG5 in Sepsis-Induced Coronary Artery Injury |
| LI Ding, LIANG Lihui, DENG Tingzhi |
| Department of Geriatrics, Hunan Provincial People's Hospital(the First Affiliated Hospital of Hunan Normal University), Changsha Hunan 410006 |
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Abstract 【Objective】 To explore the mechanism of SNHG5, a long non-coding RNA(lncRNA) associated with inflammation, in sepsis-induced coronary artery injury. 【Methods】 Ten male C57BL/6 mice were randomly divided into a sham group(Sham) and a sepsis group(Sepsis), with five mice in each group. A sepsis mouse model was established using the cecal ligation and puncture method. The expression levels of inflammation-related lncRNAs in coronary artery tissue were detected. The target genes of SNHG5 were predicted and analyzed using the starBase v2.0 database. In in-vitro experiments, mouse aortic endothelial cells(mAECs) were cultured. And 30% serum from Sham and Sepsis groups of mice was used to stimulate the mAECs. Dual-luciferase assays were used to analyze the regulatory relationship among SNHG5, miR-377-3p, and methionine aminopeptidase 2(METAP2). 【Results】 SNHG5 and METAP2 were highly expressed in the coronary arteries of Sepsis mice, while miR-377-3p was lowly expressed(P<0.05). The expression levels of miR-377-3p were negatively correlated with those of SNHG5 and METAP2(P<0.05), while SNHG5 expression was significantly positively correlated with METAP2 expression(P<0.05). Compared to Sham mice, serum from Sepsis mice significantly upregulated SNHG5 expression in mAECs(P<0.05). Serum from Sepsis mice also significantly upregulated METAP2 expression and downregulated miR-377-3p expression(P<0.05). Knockdown of SNHG5 promoted miR-377-3p expression and inhibited METAP2 expression(P<0.05).【Conclusion】 SNHG5 promotes apoptosis of mAECs induced by sepsis and may act as a competitive endogenous RNA regulator of miR-377-3p and METAP2, participating in sepsis-induced coronary artery injury.
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Received: 15 September 2025
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