作者： Tan, Ying;Lei, Cai;Tang, Huifang;Zhu, Xiao;Yi, Guanghui*

期刊： DNA AND CELL BIOLOGY,2020年39(9):1494-1505 ISSN：1044-5498

通讯作者： Yi, Guanghui

作者机构： [Lei, Cai; Tan, Ying; Yi, Guanghui; Zhu, Xiao] Univ South China, Hengyang Med Coll, Inst Cardiovasc Dis, Key Lab Atherosclerol Hunan Prov,Hunan Int Sci &, Hengyang 421001, Peoples R China.;[Tang, Huifang; Tan, Ying] Univ South China, Affiliated Hosp 1, Hengyang, Peoples R China.

通讯机构： [Yi, Guanghui] U;Univ South China, Hengyang Med Coll, Inst Cardiovasc Dis, Key Lab Atherosclerol Hunan Prov,Hunan Int Sci &, Hengyang 421001, Peoples R China.

关键词： cardiovascular diseases;mitochondrial quality control;the Hippo pathway

摘要： Mitochondria serve as a hub for cell metabolism, energy production, and reactive oxygen species generation through multiple signaling pathways that control cardiomyocyte survival and death and contribute to the pathophysiological process of cardiovascular diseases (CVDs). Therefore, maintaining mitochondrial quality control (MQC) is essential for mitochondrial homeostasis and cardiac health. The Hippo pathway is a conserved signaling cascade that regulates mitochondrial function and cardiomyocyte fate and plays a crucial role in cardiac regeneration, repair, and diseases. MQC and the Hippo pathway are tightly coupled in CVDs, and several regulatory elements of the Hippo pathway directly/indirectly regulate mitochondria-related proteins to mediate mitochondrial morphology and function. In turn, mitochondrial morphology partly influences Hippo pathway function in the heart. This review outlines the underlying mechanisms by which the Hippo pathway regulates MQC from a variety of perspectives, including mitochondrial dynamics, mitophagy, mitochondrial biogenesis, mitochondrial apoptosis under oxidative stress, and mitochondrial metabolism. We also discuss the roles of the Hippo pathway in orchestrating mitochondria in CVDs, such as myocardial ischemia-reperfusion injury, septic cardiomyopathy, and diabetic cardiomyopathy, which may provide a novel therapeutic strategy. © Copyright 2020, Mary Ann Liebert, Inc., publishers 2020.

语种： 英文

作者： Zheng, Zhi;Zeng, Yongzhi;Zhu, Xiao;Tan, Ying;Li, Yi;...

期刊： Inflammation,2019年42(2):606-617 ISSN：0360-3997

通讯作者： Yi, Guanghui

作者机构： [Li, Qian; Zheng, Zhi; Zeng, Yongzhi; Tan, Ying; Yi, Guanghui; Li, Yi; Zhu, Xiao] Univ South China, Inst Cardiovasc Res, Key Lab Atherosclerol Hunan Prov, 28 W Changsheng Rd, Hengyang 421001, Hunan, Peoples R China.

通讯机构： [Yi, Guanghui] U;Univ South China, Inst Cardiovasc Res, Key Lab Atherosclerol Hunan Prov, 28 W Changsheng Rd, Hengyang 421001, Hunan, Peoples R China.

关键词： apoM-S1P;ox-LDL;inflammatory factors;adhesion molecules;atherosclerosis

摘要： Studies have shown that apolipoprotein M (apoM), the main carrier of sphingosine-1-phosphate (S1P), is closely related to lipid metabolism and inflammation. While there are many studies on apoM and lipid metabolism, little is known about the role of apoM in inflammation. Atherosclerosis is a chronic inflammatory process. To clarify what role apoM plays in atherosclerosis, we used oxidized low-density lipoprotein (ox-LDL) to induce an inflammatory model of atherosclerosis. Our preliminary results indicate that ox-LDL upregulates the expression of S1P receptor 2 (S1PR2) in human umbilical vein endothelial cells (HUVECs). Ox-LDL-induced HUVECs were treated with apoM-bound S1P (apoM-S1P), free S1P or apoM, and apoM-S1P was found to significantly inhibit the expression of inflammatory factors and adhesion molecules. In addition, apoM-S1P inhibits ox-LDL-induced cellular inflammation via S1PR2. Moreover, apoM-S1P induces phosphorylation of phosphatidylinositol 3-kinase (PI3K)/Akt, preventing nuclear translocation of nuclear factor-κB (NF-κB). PI3K-specific inhibitors and Akt inhibitors suppress apoM-S1P/S1PR2-induced interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) release and affect nuclear translocation of NF-κB. In conclusion, the results demonstrate for the first time that apoM-S1P inhibits ox-LDL-induced inflammation in HUVECs via the S1PR2-mediated PI3K/Akt signaling pathway. This finding may aid in the development of new treatments for atherosclerosis. © 2018, Springer Science+Business Media, LLC, part of Springer Nature.

语种： 英文

作者： Zheng, Zhi;Zeng, Yong-Zhi;Ren, Kun;Zhu, Xiao;Tan, Ying;...

期刊： International Immunopharmacology,2019年66(3):224-235 ISSN：1567-5769

通讯作者： Yi, Guang-Hui

作者机构： [Li, Qian; Ren, Kun; Zheng, Zhi; Zeng, Yong-Zhi; Tan, Ying; Yi, Guang-Hui; Li, Yi; Zhu, Xiao] Univ South China, Key Lab Atherosclerol Hunan Prov, Inst Cardiovasc Dis, 28 W Changsheng Rd, Hengyang 421001, Hunan, Peoples R China.

通讯机构： [Yi, Guang-Hui] U;Univ South China, Key Lab Atherosclerol Hunan Prov, Inst Cardiovasc Dis, 28 W Changsheng Rd, Hengyang 421001, Hunan, Peoples R China.

关键词： Inflammation;Interleukin-1beta;Lymphangiogenesis;Sphingosine-1-phosphate;Tumor necrosis factor-alpha

摘要： Inflammation-induced lymphangiogenesis is a widely accepted concept. However, most of the inflammatory factors and their related mechanisms have not been clarified. It has been reported that sphingosine-1-phosphate (S1P) is not only closely related to the chronic inflammatory process but also affects angiogenesis. Therefore, we investigated the inflammatory effects of S1P on human lymphatic endothelial cells (HLECs). Our results showed that S1P promotes tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) secretion in HLECs. We also confirmed that S1P-stimulated TNF-alpha and IL-1 beta secretion is mediated through S1P receptor 1 (S1PR1). Using TNF-alpha SiRNA and IL-1 beta siRNA, we found that TNF-alpha and IL-1 beta play essential roles in S1P-induced HLEC proliferation, migration, and tube formation. Sip induces phosphorylation of NF-kappa B p65 and activation of NF-kappa B nuclear translocation. A S1PR1 antagonist (W146) and NF-kappa B inhibitor (BAY11-7082) inhibited S1P-induced TNF-alpha and IL-1 beta secretion and prevented NF-kappa B nuclear translocation. Taken together, the results demonstrated for the first time that S1P promotes the secretion of TNF-alpha and IL-1 beta in HLECs via S1PR1-mediated NF-kappa B signaling pathways, thus affecting lymphangiogenesis. The study provides a new strategy for finding treatments for lymphangiogenesis-related diseases.

语种： 英文

作者： 曾勇智;张弛;易光辉

期刊： 吉林医学,2018年39(3):597-599 ISSN：1004-0412

作者机构： 南华大学医学院机能学实验中心,湖南衡阳,421001;[张弛; 易光辉; 曾勇智] 南华大学

关键词： 开放式;医学机能实验;教学模式

摘要： 近年来,我校以“一基三实、一路三建”为发展思路,围绕创建特色鲜明的高水平教学研究型大学为目标,不断完善本科专业创新人才培养方案,深化高校课程教学模式的改革,对于专业核心课程要求全部采用研究型教学模式,倡导问题导向的学习方法,学生变被动接受为主动获取,这就要求学校构建的实践教学体系和内容须体现“以学生为本”的教学理念,学校所提供的实验平台必须是开放式的,以满足学生开展自主学习与实践创新的需要.医学作为一门实践性很强的学科,为了更好地促进资源共享,许多高等医学院校成立了机能学实验中心.

语种： 中文

作者： Zhu, Xiao;Ren, Kun;Zeng, Yong-Zhi;Zheng, Zhi;Yi, Guang-Hui*

期刊： Molecular Immunology,2018年103(4):55-62 ISSN：0161-5890

通讯作者： Yi, Guang-Hui

作者机构： [Ren, Kun; Zheng, Zhi; Zeng, Yong-Zhi; Yi, Guang-Hui; Zhu, Xiao] Univ South China, Key Lab Arteriosclerol Hunan Prov, Inst Cardiovasc Dis, 28 W Chang Sheng Rd, Hengyang 421001, Peoples R China.

通讯机构： [Yi, Guang-Hui] U;Univ South China, Key Lab Arteriosclerol Hunan Prov, Inst Cardiovasc Dis, 28 W Chang Sheng Rd, Hengyang 421001, Peoples R China.

关键词： membrane protein;sphingosine 1 phosphate;spinster 2;unclassified drug;anion transport protein;carrier protein;lysophospholipid;membrane protein;sphingolipid transporter 2, zebrafish;sphingosine;sphingosine 1-phosphate;Spns2 protein, human;zebrafish protein;drug delivery system;homeostasis;human;immune response;malignant neoplasm;nonhuman;priority journal;protein function;protein localization;protein structure;Review;signal transduction;zebra fish;analogs and derivatives;animal;cell differentiation;cell motion;cell survival;immunology;metabolism;transport at the cellular level;Animals;Anion Transport Proteins;Biological Transport;Carrier Proteins;Cell Differentiation;Cell Movement;Cell Survival;Humans;Lysophospholipids;Membrane Proteins;Sphingosine;Zebrafish;Zebrafish Proteins

摘要： Sphingosine-1-phosphate (S1P), a bioactive metabolite of sphingolipid, has an important role in lymphocyte trafficking, immune responses, vascular and embryonic development, cancer, bone homeostasis, etc. S1P is produced intracellularly and then secreted into the circulation to engage in the above physiological or pathological processes by regulating the proliferation, differentiation and survival of target cells; however, the underlying mechanisms of S1P secretion and function remain poorly understood. Recently, Spinster 2 (SPNS2), a newly identified transporter of S1P, was shown to act as a mediator of intracellular S1P release and play an important role in the regulation of S1P. In this review, we focus on the primary biological characteristics and functions of SPNS2 and provide novel insights into the development of therapies for S1P-related disorders. © 2018 Elsevier Ltd

语种： 英文

作者： 易光辉

期刊： 中国动脉硬化杂志,2018年26(10):973-979 ISSN：1007-3949

作者机构： 南华大学心血管疾病研究所南华大学衡阳医学院动脉硬化学湖南省重点实验室,湖南省衡阳市,421001;[易光辉] 南华大学

关键词： 淋巴管;动脉粥样硬化;胆固醇逆转运;炎症;免疫

摘要： 动脉粥样硬化是一种慢性炎症性疾病,是血管壁对各种损伤的异常反应。虽然影响动脉粥样硬化的因素很多,但淋巴管在动脉粥样硬化中的作用一直被忽视。传统上认为淋巴管是将间质液回流至血液循环的通道。在早期的研究中,发现动脉粥样硬化周围存在大量淋巴管,但两者之间的关系一直不清楚。近期研究发现淋巴管不仅参与动脉炎症的起始和消退,在胆固醇逆转运中也发挥着积极作用。此外,改善淋巴功能或促进局部淋巴管生成似乎可以减轻动脉粥样硬化的进展。因此,研究淋巴管与动脉粥样硬化的关系对干预动脉粥样硬化的发生发展具有重要意义。文章介绍了淋巴管与动脉粥样硬化发生发展相关的炎症、胆固醇逆转运以及免疫等因素的关系,以期为动脉粥样硬化干预策略的研究提供新的视角。

语种： 中文

作者： Ren, Kun;Zhu, Xiao;Zheng, Zhi;Mo, Zhong-Cheng;Peng, Xiao-Shan;...

期刊： Ateroskleroz,2018年270:57-67 ISSN：2078-256X

通讯作者： Yi, Guang-Hui

作者机构： [Peng, Xiao-Shan; Ren, Kun; Zheng, Zhi; Zeng, Yong-Zhi; Yi, Guang-Hui; Zhu, Xiao; Qi, Hui-Zhou] Univ South China, Key Lab Arteriosclerol Hunan Prov, Inst Cardiovasc Dis, 28 W Changsheng Rd, Hengyang City 421001, Hunan, Peoples R China.;[Mo, Zhong-Cheng; Ou, Han-Xiao] Univ South China, Dept Histol & Embryol, Hengyang 421001, Hunan, Peoples R China.;[Zhang, Qing-Hai] Univ South China, Affiliated Hosp 1, Clin Res Inst, Hengyang 421001, Hunan, Peoples R China.;[Zhao, Guo-Jun] Guilin Med Univ, Dept Histol & Embryol, Guilin 541004, Guangxi, Peoples R China.

通讯机构： [Yi, Guang-Hui] U;Univ South China, Key Lab Arteriosclerol Hunan Prov, Inst Cardiovasc Dis, 28 W Changsheng Rd, Hengyang City 421001, Hunan, Peoples R China.

关键词： acyl coenzyme A desaturase;antagomir;apolipoprotein E;cholesterol;cholesterol acyltransferase;cholesterol ester;cholesterol ester transfer protein;cholesterol ester transfer protein h 3;fatty acid synthase;free cholesterol;glycerol 3 phosphate acyltransferase;high density lipoprotein cholesterol;hydroxymethylglutaryl coenzyme A reductase;insulin induced gene 1;iodine 125;microRNA 24;protein;radiopharmaceutical agent;scavenger receptor BI;small interfering RNA;sterol regulatory element binding protein 1c;sterol regulatory element binding protein 2;triacylglycerol;tritium;tyramine cellobiose i 125;unclassified drug;high density lipoprotein cholesterol;microRNA;MIRN24 microRNA, human;Mirn24 microRNA, mouse;SCARB1 protein, human;Scarb1 protein, mouse;scavenger receptor B;3' untranslated region;animal experiment;animal model;animal tissue;Article;atherogenesis;atherosclerosis;atherosclerotic plaque;binding site;cholesterol blood level;cholesterol level;controlled study;down regulation;enzyme chemistry;flow cytometry;gene overexpression;gene repression;genetic transfection;high performance liquid chromatography;human;human cell;in vitro study;in vivo study;lipid transport;liver cell;luciferase assay;macrophage;male;mouse;nonhuman;prediction;priority journal;promoter region;real time polymerase chain reaction;triacylglycerol blood level;Western blotting;animal;apolipoprotein E knockout mouse;atherosclerosis;blood;disease model;genetics;HEK293 cell line;Hep-G2 cell line;liver;metabolism;pathology;RNA processing;THP-1 cell line;3' Untranslated Regions;Animals;Atherosclerosis;Binding Sites;Cholesterol, HDL;Disease Models, Animal;HEK293 Cells;Hep G2 Cells;Humans;Liver;Macrophages;Male;Mice, Knockout, ApoE;MicroRNAs;RNA Processing, Post-Transcriptional;Scavenger Receptors, Class B;THP-1 Cells

摘要： Background and aims: Liver scavenger receptor class B type I (SR-BI) exerts atheroprotective effects through selective lipid uptake (SLU) from high-density lipoprotein cholesterol (HDL-C). Low hepatic SR-BI expression leads to high HDL-C levels in the circulation and an increased risk of atherosclerosis. Furthermore, macrophage SR-BI mediates bidirectional cholesterol flux and may protect against atherogenesis. Previous studies have revealed that miR-24 is closely related to cardiovascular disease (CVD) progression. We aimed to investigate the molecular mechanisms by which miR-24 participates in SR-BI-mediated selective HDL cholesteryl ester (HDL-CE) uptake and further atherogenesis in apoE−/− mice. Methods: Bioinformatic predictions and luciferase reporter assays were utilized to detect the association between miR-24 and the SR-BI 3′ untranslated region (3′ UTR), and RT-PCR and western blotting were used to evaluate SR-BI mRNA and protein expression, respectively. The effects of miR-24 on Dil-HDL uptake were determined by flow cytometry assay. Double-radiolabeled HDL (125I-TC-/[3H] CEt-HDL) was utilized to measure the effects of miR-24 on HDL and CE binding and SLU in HepG2 and PMA-treated THP-1 cells. In addition, total cholesterol (TC) levels in HepG2 cells were analyzed using enzymatic methods, and macrophage lipid content was evaluated by high-performance liquid chromatography (HPLC) assay. Small interfering RNA (siRNA) and pcDNA3.1(−)-hSR-BI plasmid transfection procedures were utilized to confirm the role of SR-BI in the effects of miR-24 on Dil-HDL uptake, SLU and cholesterol levels in both cell types. Hepatic SR-BI level in apoE−/− mice was measured by western blotting. Liver TC, FC and CE levels and plasma triglycerides (TG), TC and HDL-C levels were evaluated enzymatically using commercial test kits. Atherosclerotic lesion sizes were measured using Oil Red O and hematoxylin-eosin staining. Results: miR-24 directly repressed SR-BI expression by targeting its 3′UTR. In addition, miR-24 decreased Dil-HDL uptake and SLU in HepG2 and THP-1 macrophages. In the presence of HDL, miR-24 decreased TC levels in HepG2 cells and TC, free cholesterol (FC) and CE levels in macrophages. Overexpression and down-regulation assays showed that SR-BI mediated the effects of miR-24 on Dil-HDL uptake, SLU and cholesterol levels. Lastly, miR-24 administration decreased hepatic SR-BI expression and promoted atheromatous plaque formation in apoE−/− mice, findings in line with those of our in vitro studies. Conclusions: These findings indicate that miR-24 accelerates atherogenesis by repressing SR-BI-mediated SLU from HDL-C. © 2018 Elsevier B.V.

语种： 英文

作者： Zheng, Zhi;Ren, Kun;Peng, Xiaoshan;Zhu, Xiao;Yi, Guanghui*

期刊： LYMPHATIC RESEARCH AND BIOLOGY,2018年16(6):498-506 ISSN：1539-6851

通讯作者： Yi, Guanghui

作者机构： [Ren, Kun; Zheng, Zhi; Peng, Xiaoshan; Yi, Guanghui; Zhu, Xiao] Univ South China, Inst Cardiovasc Dis, Key Lab Arteriosclerol Hunan Prov, 28 W Changsheng Rd, Hengyang City 421001, Peoples R China.

通讯机构： [Yi, Guanghui] U;Univ South China, Inst Cardiovasc Dis, Key Lab Arteriosclerol Hunan Prov, 28 W Changsheng Rd, Hengyang City 421001, Peoples R China.

关键词： chemokine receptor CCR7;gamma interferon;high density lipoprotein cholesterol;intercellular adhesion molecule 1;messenger RNA;secondary lymphoid tissue chemokine;vascular cell adhesion molecule 1;vasculotropin C;vasculotropin receptor 3;antilipemic agent;antithrombocytic agent;cholesterol;vasodilator agent;artery intima;Article;atherosclerosis;B lymphocyte;bone marrow derived macrophage;cell transdifferentiation;cholesterol transport;cytokine release;dendritic cell;disease association;disease exacerbation;drug delivery system;heart infarction;human;immunocompetent cell;inflammation;lymph node;lymph vessel;lymphangiogenesis;lymphocyte migration;macrophage migration;nonhuman;patient care;priority journal;protein expression;signal transduction;smooth muscle cell;T lymphocyte;animal;atherosclerosis;atherosclerotic plaque;drug effect;immunology;lymph vessel;lymphangiogenesis;macrophage;metabolism;pathology;transport at the cellular level;Animals;Atherosclerosis;B-Lymphocytes;Biological Transport;Cholesterol;Dendritic Cells;Disease Progression;Humans;Hypolipidemic Agents;Lymphangiogenesis;Lymphatic Vessels;Macrophages;Plaque, Atherosclerotic;Platelet Aggregation Inhibitors;T-Lymphocytes;Vasodilator Agents

摘要： Many basic and clinical studies have demonstrated that atherosclerosis is a chronic inflammatory disease. Although there are many factors affecting atherosclerosis, the role of lymphatic vessels in this disease has been neglected. Traditionally, lymphatic vessels have been considered to be passages for transporting interstitial fluid to the blood circulation. However, as early as the last century, researchers found that there are numerous lymphatic vessels surrounding sites of atherosclerosis; however, the relationship between lymphatic vessels and atherosclerosis is not clear. With further research, lymphatic vessels were determined to be involved in the induction and resolution of arterial inflammation and also to play a positive role in plaque cholesterol transport. There are abundant immune cells around atherosclerosis, and these immune cells not only have a significant impact on plaque formation but also affect local lymphangiogenesis (IAL). This promotion of IAL seems to relieve the progression of atherosclerosis. Therefore, research into the relationship between lymphatic vessels and atherosclerosis is of great importance for improving atherosclerosis treatment. This review highlights what is known about the relationship between lymphatic vessels and atherosclerosis, including the effect of immune cells on IAL, and reverse cholesterol transport. In addition, we present some of our views on the improvement of atherosclerosis treatment, which have significant clinical value in research. © 2018, Mary Ann Liebert, Inc., publishers.

语种： 英文

作者： 郑治;廖雪姣;秦雅婧;易光辉

期刊： 中国动脉硬化杂志,2018年26(10):1063-1069 ISSN：1007-3949

作者机构： 南华大学心血管疾病研究所;南华大学衡阳医学院;动脉硬化学湖南省重点实验室,湖南省衡阳市421001;[廖雪姣; 郑治; 秦雅婧; 易光辉] 南华大学

关键词： 淋巴管;高密度脂蛋白;胆固醇逆向转运;动脉粥样硬化

摘要： 细胞需要胆固醇才能生存,但过量的胆固醇对细胞具有毒性,因此细胞需要调节胆固醇的稳态。细胞内胆固醇被转运到高密度脂蛋白载脂蛋白AI,会以胆固醇逆向转运的方式返回肝脏代谢。胆固醇逆向转运不仅是维持细胞胆固醇稳态所需的生理过程,而且对动脉粥样硬化发展起到潜在的抑制作用。目前的研究主要集中在细胞胆固醇流出的最初途径和最终代谢上,但关于胆固醇是如何离开血液却知之甚少。越来越多的研究表明,在胆固醇逆向转运过程中高密度脂蛋白需要通过淋巴管转运以返回到肝脏代谢。因此,研究高密度脂蛋白从血液流入外周组织的过程,以及它是怎样通过淋巴管转运对治疗动脉粥样硬化具有重要意义。本综述主要介绍淋巴管与胆固醇逆向转运之间的联系,为治疗动脉粥样硬化性心血管疾病提供新的策略。

语种： 中文

作者： Zeng, Yongzhi;Ren, Kun;Zhu, Xiao;Zheng, Zhi;Yi, Guanghui*

期刊： Advances in Clinical Chemistry,2018年87:1-36 ISSN：0065-2423

通讯作者： Yi, Guanghui

作者机构： [Ren, Kun; Zheng, Zhi; Zeng, Yongzhi; Yi, Guanghui; Zhu, Xiao] Univ South China, Inst Cardiovasc Dis, Key Lab Arteriosclerol Hunan Prov, Hengyang, Peoples R China.

通讯机构： [Yi, Guanghui] U;Univ South China, Inst Cardiovasc Dis, Key Lab Arteriosclerol Hunan Prov, Hengyang, Peoples R China.

关键词： Adipogenesis;Dyslipidemias;Lipids metabolism;Long non-coding RNAs;Metabolic disease

摘要： Long noncoding RNAs (lncRNAs) are an important group of pervasive noncoding RNAs (>200 nt) proposed to be crucial regulators of numerous physiological and pathological processes. Through interactions with RNA, chromatin, and protein, lncRNAs modulate mRNA stability, chromatin structure, and the function of proteins (including transcription factors). In addition, to their well-known roles in the modulation of cell growth, apoptosis, neurological disease progression and cancer metastasis, these large molecules have also been identified as likely mediators of lipid metabolism. In particular, lncRNAs orchestrate adipogenesis; fatty acid, cholesterol, and phospholipid metabolism and transport; and the formation of high-density and low-density lipoproteins (HDLs and LDLs). LncRNAs also appear to target several transcription factors that play essential roles in the regulation of lipid metabolism, such as liver X receptors (LXRs), sterol regulatory element binding proteins (SREBPs), and peroxisome proliferator-activated receptor γ (PPARγ). Better understanding the regulatory roles of lncRNAs in dyslipidemia, atherosclerosis, and adipogenesis will reveal appropriate strategies to treat these diseases. In this review, we review recent progress in lncRNA-mediated regulation of lipid metabolism, as well as its role in the regulation of adipogenesis. © 2018 Elsevier Inc.

语种： 英文

作者： Ren, Kun;Lu, Yan-Ju;Mo, Zhong-Cheng;Liu, Xing;Tang, Zhen-Li;...

期刊： Journal of Physiology and Biochemistry,2017年73(2):287-296 ISSN：1138-7548

通讯作者： Yi, Guang-Hui

作者机构： [Jiang, Yue; Peng, Xiao-Shan; Ren, Kun; Yi, Guang-Hui; Tang, Zhen-Li] Univ South China, Inst Cardiovasc Dis, Key Lab Arteriosclerol Hunan Prov, 28 W Changsheng Rd, Hengyang 421001, Hunan, Peoples R China.;[Li, Li; Lu, Yan-Ju] Maternal & Child Hlth Hosp Hubei Prov, Dept Pathol, Wuhan 430072, Hubei Province, Peoples R China.;[Mo, Zhong-Cheng] Univ South China, Dept Histol & Embryol, Hengyang 421001, Hunan, Peoples R China.;[Liu, Xing] Chinese Acad Med Sci, Natl Lab Med Mol Biol, Inst Basic Med Sci, Sch Basic Med,Peking Union Med Coll, Beijing 100005, Peoples R China.;[Zhang, Qing-Hai] Univ South China, Affiliated Hosp 1, Clin Res Inst, Hengyang 421001, Hunan, Peoples R China.

通讯机构： [Yi, Guang-Hui] U;Univ South China, Inst Cardiovasc Dis, Key Lab Arteriosclerol Hunan Prov, 28 W Changsheng Rd, Hengyang 421001, Hunan, Peoples R China.

关键词： apolipoprotein A1;endothelial nitric oxide synthase;interleukin 10;interleukin 1beta;oxidized low density lipoprotein;phosphatidylinositol 3 kinase;protein kinase B;scavenger receptor B;sphingosine 1 phosphate;sphingosine 1 phosphate receptor;sphingosine 1 phosphate receptor 2;tumor necrosis factor;unclassified drug;2-hexyl-1-cyclopentanone thiosemicarbazone;AKT1 protein, human;APOA1 protein, human;apolipoprotein A1;cyclopentane derivative;IL10 protein, human;IL1B protein, human;interleukin 10;interleukin 1beta;low density lipoprotein;lysophospholipid;phosphatidylinositol 3 kinase;protein kinase B;recombinant protein;S1PR2 protein, human;SCARB1 protein, human;scavenger receptor B;sphingosine;sphingosine 1 phosphate receptor;sphingosine 1-phosphate;thiosemicarbazone derivative;TNF protein, human;tumor necrosis factor;Article;atherosclerosis;concentration response;controlled study;cytokine release;endothelial dysfunction;enzyme activation;enzyme linked immunosorbent assay;human;human cell;in vitro study;inflammation;protein expression;signal transduction;time;umbilical vein endothelial cell;Western blotting;agonists;analogs and derivatives;antagonists and inhibitors;cell culture;chemistry;cytology;drug effects;gene expression regulation;genetics;immunology;kinetics;metabolism;nucleocytoplasmic transport;signal transduction;umbilical vein endothelial cell;vascular endothelium;Active Transport, Cell Nucleus;Apolipoprotein A-I;Cells, Cultured;Cyclopentanes;Endothelium, Vascular;Gene Expression Regulation;Human Umbilical Vein Endothelial Cells;Humans;Interleukin-10;Interleukin-1beta;Kinetics;Lipoproteins, LDL;Lysophospholipids;Phosphatidylinositol 3-Kinase;Proto-Oncogene Proteins c-akt;Receptors, Lysosphingolipid;Recombinant Proteins;Scavenger Receptors, Class B;Signal Transduction;Sphingosine;Thiosemicarbazones;Tumor Necrosis Factor-alpha

摘要： Endothelial dysfunction plays a vital role during the initial stage of atherosclerosis. Oxidized low-density lipoprotein (ox-LDL) induces vascular endothelial injury and vessel wall inflammation. Sphingosine-1-phosphate (S1P) exerts numerous vasoprotective effects by binding to diverse S1P receptors (S1PRs; S1PR1-5). A number of studies have shown that in endothelial cells (ECs), S1PR2 acts as a pro-atherosclerotic mediator by stimulating vessel wall inflammation through the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway. Scavenger receptor class B member I (SR-BI), a high-affinity receptor for apolipoprotein A-I (apoA-I)/high-density lipoprotein (HDL), inhibits nuclear factor-κB (NF-κB) translocation and decreases the plasma levels of inflammatory mediators via the PI3K/Akt pathway. We hypothesized that the inflammatory effects of S1P/S1PR2 on ECs may be regulated by apoA-I/SR-BI. The results showed that ox-LDL, a pro-inflammatory factor, augmented the S1PR2 level in human umbilical vein endothelial cells (HUVECs) in a dose- and time-dependent manner. In addition, S1P/S1PR2 signaling influenced the levels of inflammatory factors, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-10, aggravating inflammation in HUVECs. Moreover, the pro-inflammatory effects induced by S1P/S1PR2 were attenuated by SR-BI overexpression and enhanced by an SR-BI inhibitor, BLT-1. Further experiments showed that the PI3K/Akt signaling pathway was involved in this process. Taken together, these results demonstrate that apoA-I/SR-BI negatively regulates S1P/S1PR2-mediated inflammation in HUVECs by activating the PI3K/Akt signaling pathway. © 2017, University of Navarra.

语种： 英文

作者： Ren, Kun;Mo, Zhong-Cheng;Liu, Xing;Tang, Zhen-Li;Jiang, Yue;...

期刊： Lipids,2017年52(2):109-117 ISSN：0024-4201

通讯作者： Yi, Guang-Hui

作者机构： [Jiang, Yue; Peng, Xiao-Shan; Ren, Kun; Shi, Jin-Feng; Yi, Guang-Hui; Tang, Zhen-Li] Univ South China, Inst Cardiovasc Dis, Key Lab Arteriosclerol Hunan Prov, 28 W Changsheng Rd, Hengyang 421001, Hunan, Peoples R China.;[Shi, Jin-Feng; Mo, Zhong-Cheng] Univ South China, Dept Histol & Embryol, Hengyang 421001, Hunan, Peoples R China.;[Liu, Xing] Chinese Acad Med Sci, Inst Basic Med Sci, Sch Basic Med, Natl Lab Med Mol Biol,Peking Union Med Coll, Beijing 100005, Peoples R China.;[Zhang, Qing-Hai] Univ South China, Affiliated Hosp 1, Clin Res Inst, Hengyang 421001, Hunan, Peoples R China.

通讯机构： [Yi, Guang-Hui] U;Univ South China, Inst Cardiovasc Dis, Key Lab Arteriosclerol Hunan Prov, 28 W Changsheng Rd, Hengyang 421001, Hunan, Peoples R China.

关键词： ApoM;TGF-β;TAK-1;JNK;C-Jun

摘要： Apolipoprotein M (apoM) is a relatively novel apolipoprotein that plays pivotal roles in many dyslipidemia-associated diseases; however, its regulatory mechanisms are poorly understood. Many cytokines have been identified that down-regulate apoM expression in HepG2 cells, among which transforming growth factor-β (TGF-β) exerts the most potent effects. In addition, c-Jun, a member of the activated protein 1 (AP-1) family whose activity is modulated by c-Jun N-terminal kinase (JNK), decreases apoM expression at the transcriptional level by binding to the regulatory element in the proximal apoM promoter. In this study, we investigated the molecular mechanisms through which TGF-β decreases the apoM level in HepG2 cells. The results revealed that TGF-β inhibited apoM expression at both the mRNA and protein levels in a dose- and time-dependent manner and that it suppressed apoM secretion. These effects were attenuated by treatment of cells with either SP600125 (JNK inhibitor) or c-Jun siRNA. 5Z-7-oxozeaenol [(a TGF-β-activated kinase 1 (TAK-1) inhibitor)] also attenuated the TGF-β-mediated inhibition of apoM expression and suppressed the activation of JNK and c-Jun. These results have demonstrated that TGF-β suppresses apoM expression through the TAK-1-JNK-c-Jun pathway in HepG2 cells. © 2016, AOCS.

语种： 英文

作者： 江悦;田梦翔;王双;易光辉

期刊： 中国动脉硬化杂志,2017年25(4):411-416 ISSN：1007-3949

作者机构： 南华大学心血管疾病研究所 动脉硬化学湖南省重点实验室,湖南省衡阳市,421001;[田梦翔; 江悦] 南华大学

关键词： 外泌体;动脉粥样硬化;微小RNA

摘要： 动脉粥样硬化是一种慢性炎症性疾病。临床上使用的抗动脉粥样硬化药物的目标主要集中在减少循环低密度脂蛋白水平,升高高密度脂蛋白水平,并减轻炎症。然而,心血管疾病的发病率和死亡率仍然很高。因此,识别未知的治疗靶点和开发新的抗动脉粥样硬化药物的需求越来越大。外泌体是活细胞分泌的来源于晚期核内体（也称为多囊泡体）的膜性囊泡。外泌体内含有与来源细胞相关的蛋白质、rRNA和微小RNA,并能够通过生物屏障,从而发挥各种生物学功能。外泌体有望成为一种治疗动脉粥样硬化的新型给药途径及基因治疗载体。

语种： 中文

作者： 赵战芝;谭健苗;张弛;易光辉

期刊： 中国高等医学教育,2016年(5):106-107 ISSN：1002-1701

作者机构： 南华大学医学院,湖南衡阳,421001;[赵战芝; 张弛; 易光辉; 谭健苗] 南华大学

关键词： 机能实验学;任务教学法;教学效果

摘要： 目的：探讨任务教学法在机能实验学教学中的应用效果。方法：以2012级临床医学专业部分学生为研究对象，对照组采用传统教学法授课，实验组采用任务教学法授课，以实验成绩和问卷调查评估教学效果。结果：实验组的总成绩和优秀率、学生的学习兴趣、自主学习能力及对教学法的满意度均高于对照组。结论：任务教学法可显著提升机能实验学的教学效果。

语种： 中文

作者： Mo, Zhong-Cheng;Ren, Kun;Liu, Xing;Tang, Zhen-Li;Yi, Guang-Hui*

期刊： Advanced Drug Delivery Reviews,2016年106(10):132-147 ISSN：0169-409X

通讯作者： Yi, Guang-Hui

作者机构： [Ren, Kun; Mo, Zhong-Cheng; Yi, Guang-Hui; Tang, Zhen-Li] Univ South China, Key Lab Arteriosclerol Hunan Prov, Inst Cardiovasc Dis, Hengyang City 421001, Hunan, Peoples R China.;[Mo, Zhong-Cheng] Univ South China, Dept Histol & Embryol, Hengyang 421001, Hunan, Peoples R China.;[Liu, Xing] Chinese Acad Med Sci, Sch Basic Med, Peking Union Med Coll, Natl Lab Med Mol Biol,Inst Basic Med Sci, Beijing 100005, Peoples R China.;[Yi, Guang-Hui] Univ South China, Inst Cardiovasc Dis, Key Lab Arteriosclerol Hunan Prov, 28 W Changsheng Rd, Hengyang 421001, Hunan, Peoples R China.

通讯机构： [Yi, Guang-Hui] U;Univ South China, Inst Cardiovasc Dis, Key Lab Arteriosclerol Hunan Prov, 28 W Changsheng Rd, Hengyang 421001, Hunan, Peoples R China.

关键词： *Drug delivery;*HDL;*Nanoparticles;*Reconstitution

摘要： High-density lipoprotein (HDL) is a comparatively dense and small lipoprotein that can carry lipids as a multifunctional aggregate in plasma. Several studies have shown that increasing the levels or improving the functionality of HDL is a promising target for treating a wide variety of diseases. Among lipoproteins, HDL particles possess unique physicochemical properties, including naturally synthesized physiological components, amphipathic apolipoproteins, lipid-loading and hydrophobic agent-incorporating characteristics, specific protein–protein interactions, heterogeneity, nanoparticles, and smaller size. Recently, the feasibility and superiority of using HDL particles as drug delivery vehicles have been of great interest. In this review, we summarize the structure, constituents, biogenesis, remodeling, and reconstitution of HDL drug delivery systems, focusing on their delivery capability, characteristics, applications, manufacturing, and drug-loading and drug-targeting characteristics. Finally, the future prospects are presented regarding the clinical application and challenges of using HDL as a pharmacodelivery carrier. © 2016 Elsevier B.V.

语种： 英文

作者： Liu, Xing;Ren, Kun;Suo, Rong;Xiong, Sheng-Lin;Zhang, Qing-Hai;...

期刊： Journal of Physiology and Biochemistry,2016年72(4):657-667 ISSN：1138-7548

通讯作者： Yi, Guang-Hui

作者机构： [Jiang, Yue; Peng, Xiao-Shan; Liu, Xing; Ren, Kun; Yi, Guang-Hui; Suo, Rong; Tang, Zhen-Li] Univ South China, Inst Cardiovasc Dis, Key Lab Arteriosclerol Hunan Prov, 28 W Changsheng Rd, Hengyang City 421001, Hunan, Peoples R China.;[Xiong, Sheng-Lin] You Country Peoples Hosp, Zhuzhou 412300, Hunan, Peoples R China.;[Zhang, Qing-Hai] Univ South China, Affiliated Hosp 1, Clin Res Inst, Hengyang 421001, Hunan, Peoples R China.;[Mo, Zhong-Cheng] Univ South China, Inst Cardiovasc Res, Life Sci Res Ctr, Key Lab Atherosclerol Hunan Prov, Hengyang 421001, Hunan, Peoples R China.

通讯机构： [Yi, Guang-Hui] U;Univ South China, Inst Cardiovasc Dis, Key Lab Arteriosclerol Hunan Prov, 28 W Changsheng Rd, Hengyang City 421001, Hunan, Peoples R China.

关键词： S1P;SR-BI;ABCA1;SphK;S1P receptors;Release

摘要： Sphingosine-1-phosphate (S1P), which has emerged as a pivotal signaling mediator that participates in the regulation of multiple cellular processes, is derived from various cells, including vascular endothelial cells. S1P accumulates in lipoproteins, especially HDL, and the majority of free plasma S1P is bound to HDL. We hypothesized that HDL-associated S1P is released through mechanisms associated with the HDL maturation process. ApoA-I, a major HDL apolipoprotein, is a critical factor for nascent HDL formation and lipid trafficking via ABCA1. Moreover, apoA-I is capable of promoting bidirectional lipid movement through SR-BI. In the present study, we confirmed that apoA-I can facilitate the production and release of S1P by HUVECs. Furthermore, we demonstrated that ERK1/2 and SphK activation induced by apoA-I is involved in the release of S1P from HUVECs. Inhibitor and siRNA experiments showed that ABCA1 and SR-BI are required for S1P release and ERK1/2 phosphorylation induced by apoA-I. However, the effects triggered by apoA-I were not suppressed by inhibiting ABCA1/JAK2 or the SR-BI/Src pathway. S1P released due to apoA-I activation can stimulate the (ERK1/2)/SphK1 pathway through S1PR (S1P receptor) 1/3. These results indicated that apoA-I not only promotes S1P release through ABCA1 and SR-BI but also indirectly activates the (ERK1/2)/SphK1 pathway by releasing S1P to trigger their receptors. In conclusion, we suggest that release of S1P induced by apoA-I from endothelial cells through ABCA1 and SR-BI is a self-positive-feedback process: apoA-I-(ABCA1 and SR-BI)-(S1P release)-S1PR-ERK1/2-SphK1-(S1P production)-(more S1P release induced by apoA-I).

语种： 英文

作者： Ren, Kun;Tang, Zhen-Li;Jiang, Yue;Tan, Yan-Mei;Yi, Guang-Hui*

期刊： Clinica Chimica Acta,2015年446:21-29 ISSN：0009-8981

通讯作者： Yi, Guang-Hui

作者机构： [Jiang, Yue; Ren, Kun; Tan, Yan-Mei; Yi, Guang-Hui; Tang, Zhen-Li] Univ South China, Inst Cardiovasc Dis, Key Lab Arteriosclerol Hunan Prov, Hengyang City 421001, Hunan, Peoples R China.;[Yi, Guang-Hui] Univ South China, Inst Cardiovasc Dis, Key Lab Arteriosclerol Hunan Prov, 28 W Chang Sheng Rd, Hengyang 421001, Hunan, Peoples R China.

通讯机构： [Yi, Guang-Hui] U;Univ South China, Inst Cardiovasc Dis, Key Lab Arteriosclerol Hunan Prov, 28 W Chang Sheng Rd, Hengyang 421001, Hunan, Peoples R China.

关键词： Apolipoprotein M;Function;Regulation

摘要： Apolipoprotein M (ApoM) is a novel apolipoprotein that was discovered in 1999 and is bound primarily to high-density lipoproteins (HDLs) in the plasma. Multiple factors may influence its expression at both the post-transcriptional and the transcriptional levels both in vivo and ex vivo as follows: hepatocyte nuclear factor-1 alpha, 4 alpha (HNF-1 alpha, 4 alpha), liver receptor homolog-1 (LRH-1), forkhead box A2 (Foxa2) and platelet activating factor (PAF) upregulate its expression; liver X receptor (LXR), retinoid X receptor (RXR), famesoid X receptor (FXR), small heterodimer partner (SHP) and the majority of cytokines downregulate its expression. However, mechanisms underlying these processes remain unknown. Structurally, there exists a characterized hydrophobic binding pocket within the apoM protein, which enables it to bind functional lipids such as Sphingosine-1-Phosphate (S1P). Functionally, it facilitates the formation of pre beta-HDL and enhances an avalanche of atheroprotective effects exerted by HDL. Moreover, in patients with diabetes, the levels of plasma apoM may decrease, whereas the augmentation of apoM decreases plasma glucose levels and magnifies the secretion of insulin. This article offers a panorama of the progress made in the research regarding the characteristics of apoM, particularly the regulation of its expression and its functions. (C) 2015 Elsevier B.V. All rights reserved.

语种： 英文

作者： Mo Zhong-Cheng;Ou Han-Xiao;Yi Guang-Hui*

期刊： 生物化学与生物物理进展,2015年42(9):788-795 ISSN：1000-3282

通讯作者： Yi Guang-Hui

作者机构： [Mo Zhong-Cheng; Ou Han-Xiao] Univ South China, Dept Histol & Embryol, Hengyang 421001, Peoples R China.;[Yi Guang-Hui] Univ South China, Key Lab Atherosclerol Hunan Prov, Inst Cardiovasc Dis, Hengyang 421001, Peoples R China.

通讯机构： [Yi Guang-Hui] U;Univ South China, Key Lab Atherosclerol Hunan Prov, Inst Cardiovasc Dis, Hengyang 421001, Peoples R China.

关键词： 载脂蛋白A-Ⅰ;高密度脂蛋白;胆固醇流出;基因突变

摘要： 高密度脂蛋白（HDL）生物合成是一个有多种膜蛋白和胞质蛋白参与的复杂过程,载脂蛋白A-Ⅰ（apo A-Ⅰ）是HDL中最主要的结构和功能蛋白,它能活化卵磷脂胆固醇脂酰基转移酶（LCAT）,贫脂apo A-Ⅰ也是巨噬细胞中三磷酸腺苷结合盒转运体A1（ABCA1）介导的胆固醇流出的重要接受体.因此,apo A-Ⅰ在HDL及胆固醇代谢中的作用至关重要,它赋予了HDL多种抗动脉粥样硬化活性.本文主要就HDL生物合成及apo A-Ⅰ在其中的作用作一综述,以期为揭示HDL的代谢机制提供新思路.

语种： 中文

作者： Wu, Rong;Zhang, Qing-Hai;Lu, Yan-Ju;Ren, Kun;Yi, Guang-Hui*

期刊： DNA AND CELL BIOLOGY,2015年34(1):6-18 ISSN：1044-5498

通讯作者： Yi, Guang-Hui

作者机构： [Ren, Kun; Wu, Rong; Lu, Yan-Ju; Yi, Guang-Hui] Univ South China, Inst Cardiovasc Res, Key Lab Atherosclerol Hunan Prov, Hengyang 421001, Hunan, Peoples R China.;[Zhang, Qing-Hai] Univ South China, Affiliated Hosp 1, Clin Res Inst, Hengyang 421001, Hunan, Peoples R China.

通讯机构： [Yi, Guang-Hui] U;Univ South China, Inst Cardiovasc Res, Key Lab Atherosclerol Hunan Prov, Hengyang 421001, Hunan, Peoples R China.

关键词： Transcription

摘要： The X-box binding protein 1 (XBP1) is not only an important component of the unfolded protein response (UPR), but also an important nuclear transcription factor. Upon endoplasmic reticulum stress, XBP1 is spliced by inositol-requiring enzyme 1 (IRE1), thereby generating functional spliced XBP1 (XBP1s). XBP1s functions by translocating into the nucleus to initiate transcriptional programs that regulate a subset of UPR- and non-UPR-associated genes involved in the pathophysiological processes of various diseases. Recent reports have implicated XBP1 in metabolic diseases. This review summarizes the effects of XBP1-mediated regulation on lipid metabolism, glucose metabolism, obesity, and atherosclerosis. Additionally, for the first time, we present XBP1s-dependent transcriptional reprogramming in metabolic diseases under different conditions, including pathology and physiology. Understanding the function of XBP1 in metabolic diseases may provide a basic knowledge for the development of novel therapeutic targets for ameliorating these diseases.

语种： 英文

作者： Qiao, Yuncheng;Guo, Dongming;Meng, Lei;Liu, Qingnan;Liu, Xiaohui;...

期刊： MOLECULAR MEDICINE REPORTS,2015年12(3):3599-3606 ISSN：1791-2997

通讯作者： Yuan, Zhonghua

作者机构： [Meng, Lei; Tang, Chaoke; Yin, Weidong; Qiao, Yuncheng; Yi, Guanghui; Guo, Dongming; Wang, Zuo; Yuan, Zhonghua] Univ South China, Inst Cardiovasc Dis, Key Lab Arteriosclerol Hunan, Hengyang 421001, Hunan, Peoples R China.;[Qiao, Yuncheng] Pingyu Renmin Hosp, Dept Cardiovasc Med, Pingyu 463400, Henan, Peoples R China.;[Liu, Qingnan] Yiyang Med Coll, Dept Basic Nursing, Yiyang 413000, Hunan, Peoples R China.;[Liu, Xiaohui] Soochow Univ, Cyrus Tang Hematol Ctr Res Partnership, Jiangsu Inst Hematol, Affiliated Hosp 1, Suzhou 215400, Jiangsu, Peoples R China.;[Tian, Guoping] Univ South China, Dept Cardiovasc Med, Affiliated Hosp 2, Hengyang 421001, Hunan, Peoples R China.

通讯机构： [Yuan, Zhonghua] U;Univ South China, Inst Cardiovasc Dis, Key Lab Arteriosclerol Hunan, 28 West Changsheng Rd, Hengyang 421001, Hunan, Peoples R China.

关键词： acyl coenzyme A;adipophilin;cholesterol acyltransferse 1;cholesterol ester;oxidized low density lipoprotein;protein kinase C alpha;unclassified drug;Acat1 protein, mouse;acetyl coenzyme A acetyltransferase;cholesterol ester;low density lipoprotein;membrane protein;oxidized low density lipoprotein;perilipin 2;protein kinase C alpha;small interfering RNA;animal cell;Article;controlled study;enzyme phosphorylation;genetic transfection;macrophage;mouse;nonhuman;polyacrylamide gel electrophoresis;protein expression;protein function;signal transduction;upregulation;animal;gene expression regulation;genetics;macrophage;metabolism;RAW 264.7 cell line;RNA interference;Acetyl-CoA C-Acetyltransferase;Animals;Cholesterol Esters;Gene Expression Regulation;Lipoproteins, LDL;Macrophages;Membrane Proteins;Mice;Protein Kinase C-alpha;RAW 264.7 Cells;RNA Interference;RNA, Small Interfering;Signal Transduction

摘要： Oxidized low-density lipoprotein (ox-LDL) can increase the expression of adipophilin and the accumulation of intracellular lipid droplets. However, the detailed mechanisms remain to be fully elucidated. The present study aimed to investigate the mechanism underlying the effect of ox-LDL on the expression of adipophilin and the accumulation of intracellular cholesterol esters. The results revealed that ox-LDL increased the activation of protein kinase C α (PKCα), expression of adipophilin and acyl-coenzymeA: cholesterol acyltransferse 1 (ACAT1) and increased accumulation of intracellular cholesterol esters. In addition, PKCα siRNA abrogated ox-LDL-induced adipophilin, expression of ATAC1 and accumulation of cholesterol esters. Furthermore, ox-LDL increased the accumulation of intracellular cholesterol esters and expression of ACAT1, and this effect were reversed by transfection with adipophilin siRNA. Taken together, these results demonstrated that ox-LDL induces the accumulation of cholesterol esters, which is mediated by the PKCα-adipophilin-ACAT1 pathway.

语种： 英文