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| 1 | 细胞内胆固醇水平调节研究进展显示文摘细胞内胆固醇水平动态平衡是细胞发挥生理功能的重要保障。破坏细胞内胆固醇水平动态平衡不仅增加心血管系统疾病患病风险,而且与许多代谢性疾病相关。细胞内胆固醇水平主要受胆固醇生物合成、摄取、流出和酯化的调节。3-羟基-3-甲基-戊二酰基辅酶A还原酶、角鲨烯单加氧酶和固醇调节元件结合蛋白2是胆固醇合成关键因子。尼曼-匹克C1型类似蛋白1、低密度脂蛋白受体和B族清道夫受体1是细胞摄取胆固醇的重要受体。三磷酸腺苷结合盒转运体A1、G1、G5/8和载脂蛋白A-I结合蛋白介导细胞内胆固醇流出。酰基辅酶A∶胆固醇酰基转移酶(ACAT)能酯化细胞内游离胆固醇。本文主要综述以上对细胞内胆固醇水平平衡有重要调节作用的关键因子研究新进展,以期为细胞内胆固醇水平调节提供新的靶点和研究方向。 | 张强 许璨 唐朝克 | 2022 | 生物化学与生物物理进展2022，49，2： | 5 |
| 2 | microRNA-125a靶向sortilin抑制巨噬细胞脂质蓄积与主动脉粥样硬化病变机制研究显示文摘目的探讨miR-125a对巨噬细胞脂质代谢及主动脉粥样硬化(atherosclerosis,AS)病变的影响及作用机制。方法油红O及比色法检测巨噬细胞内脂滴情况及脂质含量;生物信息学预测miR-125a下游靶标;双荧光素酶报告基因验证miR-125a与sortilin mRNA靶向结合;qPCR、Western blot和免疫组化检测荷脂THP-1巨噬细胞和低密度脂蛋白受体敲除(LDLR−/−)小鼠中miR-125a及sortilin表达;全自动生化分析仪测定血脂改变;组织染色显示主动脉AS斑块面积及脂质沉积情况。结果过表达miR-125a可减轻THP-1巨噬细胞内脂质蓄积;生信分析和荧光素酶报告基因显示sortilin mRNA是miR-125a的作用靶标;过表达miR-125a可下调巨噬细胞sortilin表达,减少胞内脂滴数量及脂质含量,改善LDLR−/−小鼠血脂谱,抑制主动脉脂质沉积及AS病变面积。结论miR-125a可通过下调sortilin表达抑制巨噬细胞脂质蓄积及主动脉AS病变。 | 吕运成 明新月 刘芳 陈诗芮 彭田红 欧阳曙晖 | 2023 | 中国临床解剖学杂志2023，41，4： | 0 |
| 3 | Sortilin-induced lipid accumulation and atherogenesis are suppressed by HNF1b SUMOylation promoted by flavone of Polygonatum odoratum显示文摘This study aims to investigate the impact of hepatocyte nuclear factor 1β(HNF1b)on macrophage sortilin-mediated lipid metabolism and aortic atherosclerosis and explore the role of the flavone of Polygonatum odoratum(PAOA-flavone)-promoted small ubiquitin-related modifier(SUMO)modification in the atheroprotective efficacy of HNF1b.HNF1b was predicted to be a transcriptional regulator of sortilin expression via bioinformatics,dual-luciferase reporter gene assay,and chromatin immunoprecipitation.HNF1b overexpression decreased sortilin expression and cellular lipid contents in THP-1 macrophages,leading to a depression in atherosclerotic plaque formation in low-density lipoprotein(LDL)receptor-deficient(LDLR−/−)mice.Multiple SUMO1-modified sites were identified on the HNF1b protein and co-immunoprecipitation confirmed its SUMO1 modification.The SUMOylation of HNF1b protein enhanced the HNF1b-inhibited effect on sortilin expression and reduced lipid contents in macrophages.PAOA-flavone treatment promoted SUMO-activating enzyme subunit 1(SAE1)expression and SAE1-catalyzed SUMOylation of the HNF1b protein,which prevented sortilin-mediated lipid accumulation in macrophages and the formation of atherosclerotic plaques in apolipoprotein E-deficient(ApoE−/−)mice.Interference with SAE1 abrogated the improvement in lipid metabolism in macrophage cells and atheroprotective efficacy in vivo upon PAOA-flavone administration.In summary,HNF1b transcriptionally suppressed sortilin expression and macrophage lipid accumulation to inhibit aortic lipid deposition and the development of atherosclerosis.This anti-atherosclerotic effect was enhanced by PAOA-flavone-facilitated,SAE1-catalyzed SUMOylation of the HNF1b protein. | Fang LIU Shirui CHEN Xinyue MING Huijuan LI Zhaoming ZENG Yuncheng LV | 2023 | Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)2023，24，11： | 0 |
| 4 | Sortilin促进心血管疾病的研究进展显示文摘Sortilin是由人SORT1基因编码的分拣蛋白,分选、运输细胞内相关蛋白底物。Sortilin不仅参与脂蛋白代谢升高血脂促进巨噬细胞内脂质蓄积与泡沫细胞形成,而且通过调控细胞因子分泌及免疫细胞间相互作用促进炎症反应。Sortilin经翻译后修饰及其介导细胞分化还可促进血管壁及瓣膜钙化。此外,Sortilin调控鞘磷脂代谢相关酶的胞内运输促进氧化应激。Sortilin主要通过增加内皮氧化应激损害血管舒缩功能导致高血压,还可通过促进动脉内皮下脂质蓄积、炎性细胞浸润及动脉壁钙盐沉着促进动脉粥样硬化性心血管疾病,并且能通过促进外周血管钙化与糖脂代谢紊乱引发微循环障碍,进而促进糖尿病外周血管疾病。总之,Sortilin在心血管疾病的发生发展中发挥重要致病作用,并具备潜在干预价值。 | 李慧娟 刘芳 陈诗芮 明新月 吕运成 | 2023 | 华夏医学2023，36，5： | 0 |
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