Previous studies have shown that miR-210-3p is involved in the development and progression of atherosclerosis, but its specific mechanisms are still unclear. This study aims to reveal the mechanism of miR-210-3p and its target genes in macrophage lipid deposition and inflammatory response, and provide new ideas for the treatment of atherosclerosis. We found miR-210-3p increased sharply in the first 12 h induced by higher doses of ox-LDL in THP-1 macrophages and then gradually decreased. MiR-210-3p mimic transfection inhibited lipid uptake and inflammatory cytokine production in ox-LDL-induced macrophages. By inhibiting IGF2/IGF2R, miR-210-3p suppressed the expression of fatty acid transcriptase CD36 and transcription factor NF-κB in ox-LDL-induced macrophages. In conclusion, miR-210-3p inhibits the expression of CD36 and NF-κB by inhibiting IGF2 / IGF2R, thereby reducing lipid accumulation and inflammatory response in ox-LDL-induced macrophages. Enhancing miR-210-3p expression may be a new strategy for the treatment of atherosclerosis.

中文翻译：

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MiR-210-3p通过抑制IGF2减轻动脉粥样硬化中的脂质蓄积和炎症。

先前的研究表明，miR-210-3p参与动脉粥样硬化的发生和发展，但其具体机​​制仍不清楚。本研究旨在揭示miR-210-3p及其靶基因在巨噬细胞脂质沉积和炎症反应中的作用机制，为动脉粥样硬化的治疗提供新的思路。我们发现，在高剂量的THP-1巨噬细胞中，高剂量的ox-LDL诱导miR-210-3p在最初的12 h急剧增加，然后逐渐降低。MiR-210-3p模拟转染抑制了ox-LDL诱导的巨噬细胞的脂质摄取和炎性细胞因子的产生。通过抑制IGF2 / IGF2R，miR-210-3p抑制了ox-LDL诱导的巨噬细胞中脂肪酸转录酶CD36和转录因子NF-κB的表达。综上所述，miR-210-3p通过抑制IGF2 / IGF2R来抑制CD36和NF-κB的表达，从而减少ox-LDL诱导的巨噬细胞的脂质蓄积和炎症反应。增强miR-210-3p表达可能是治疗动脉粥样硬化的新策略。