Gene · 2026
Molecular mechanism of the LncRNA MALAT1/NF-κB signaling pathway in mediating vascular endothelial injury under glucose and lipid metabolism disorders.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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Aihemaiti Gulandanmu, Liu Fen, Song Ning, Zhao Long, Xie Qian, Adili Niyaziaili, Pi Qixing, Zhang Chenle, Ji Wei, Xieyire Hamulati, Fang Bin Bin, Yang Yining, Li XiaoMei
Аннотация
BACKGROUND: Disordered glucose and lipid metabolism exacerbates endothelial injury, promoting atherosclerosis (AS). This study aimed to elucidate the role of the lncRNA MALAT1 in endothelial injury under high glucose and palmitic acid (HGPA) conditions via in vivo and in vitro experiments.
METHODS: Bioinformatics identified MALAT1 as a key regulator. Functional assays, RIPpull, and Western blotting assessed its role in inflammation, apoptosis, and ferroptosis. Animal and clinical studies (100 AS patients vs. 100 controls) validated the findings.
RESULTS: MALAT1 was upregulated by HGPA, activating NF-κB, increasing inflammation, and promoting ferroptosis. MALAT1 knockdown or NF-κB inhibition attenuated these effects. Clinically, circulating MALAT1 correlated with inflammatory markers and endothelial dysfunction.
CONCLUSIONS: MALAT1 mediates endothelial injury in AS via NF-κB, highlighting its potential as a diagnostic biomarker and therapeutic target for atherosclerosis with glucolipid disorders. Disordered glucose and lipid metabolism exacerbates endothelial injury, thereby promoting the development of atherosclerosis (AS).
METHODS: Bioinformatics identified MALAT1 as a key regulator. Functional assays, RIPpull, and Western blotting assessed its role in inflammation, apoptosis, and ferroptosis. Animal and clinical studies (100 AS patients vs. 100 controls) validated the findings.
RESULTS: MALAT1 was upregulated by HGPA, activating NF-κB, increasing inflammation, and promoting ferroptosis. MALAT1 knockdown or NF-κB inhibition attenuated these effects. Clinically, circulating MALAT1 correlated with inflammatory markers and endothelial dysfunction.
CONCLUSIONS: MALAT1 mediates endothelial injury in AS via NF-κB, highlighting its potential as a diagnostic biomarker and therapeutic target for atherosclerosis with glucolipid disorders. Disordered glucose and lipid metabolism exacerbates endothelial injury, thereby promoting the development of atherosclerosis (AS).