靶向CD36调控脂质代谢:糖尿病心肌病防治新靶点
作者:
  • 周嘉琪 1

    周嘉琪

    广东医科大学附属医院麻醉科,广东省湛江市 524000
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  • 林介夫 1

    林介夫

    广东医科大学附属医院麻醉科,广东省湛江市 524000
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  • 陈嘉佳 1

    陈嘉佳

    广东医科大学附属医院麻醉科,广东省湛江市 524000
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  • 谢林 1

    谢林

    广东医科大学附属医院麻醉科,广东省湛江市 524000
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  • 夏正远 1,2,3

    夏正远

    广东医科大学附属医院麻醉科,广东省湛江市 524000;香港大学生物医药技术国家重点实验室,香港 999077;湖北省钟祥市官冲博士塆科研与转化培训平台,湖北省钟祥市 431900 [专家简介] 夏正远,广东医科大学附属医院麻醉科特聘教授,香港大学生物医药技术国家重点实验室研究员,澳门科技大学中医学院中西医结合专业博士研究生导师,中国心胸血管麻醉学会理事,加州大学戴维斯分校志愿临床教授。 2004年在加拿大不列颠哥伦比亚大学获麻醉学与药理学及治疗学医学博士学位,先后于1998年在美国印第安纳大学Krannert心脏研究所、1999年在比利时鲁汶大学麻醉与外科实验中心及2004─2006年在加拿大不列颠哥伦比亚大学药学院等处作访问或博士后研究。曾先后在武汉大学和中山大学的附属医院麻醉科及香港大学麻醉学系工作。主要从事心肌缺血再灌注损伤研究,在Anesthesiology、Cell Metabolism、Diabetes、Intensive Care Medicine、Critical Care Medicine、Free Radical Biology and Medicine、European Heart Journal及Circulation等发表SCI研究论文260余篇3篇在Web of Science上高引,论文被引用26 220余次,H-index 60。曾主持8项香港研究资助局基金课题、1项国际心血管麻醉师学会课题、1项香港政府医疗卫生研究基金、1项香港AoE卓越科学领域分课题,另外主持6项国家自然科学基金课题。担任Lancet、Lancet Digit Health、Diabetes、Redox Biology、EClinicalMedicine等30多种学术期刊审稿人及加拿大、瑞士、克罗地亚、中国国家科研基金课题评审专家。发表的论文{XIA Z, HUANG Z, ANSLEY D M.Large-dose propofol during cardiopulmonary bypass decreases biochemical markers of myocardial injury in coronary surgery patients:a comparison with isoflurane.Anesth Analg, 6,33:527-53
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作者单位:

(1.广东医科大学附属医院麻醉科,广东省湛江市 524000;2.香港大学生物医药技术国家重点实验室,香港 999077;3.湖北省钟祥市官冲博士塆科研与转化培训平台,湖北省钟祥市 431900) [专家简介] 夏正远,广东医科大学附属医院麻醉科特聘教授,香港大学生物医药技术国家重点实验室研究员,澳门科技大学中医学院中西医结合专业博士研究生导师,中国心胸血管麻醉学会理事,加州大学戴维斯分校志愿临床教授。 2004年在加拿大不列颠哥伦比亚大学获麻醉学与药理学及治疗学医学博士学位,先后于1998年在美国印第安纳大学Krannert心脏研究所、1999年在比利时鲁汶大学麻醉与外科实验中心及2004─2006年在加拿大不列颠哥伦比亚大学药学院等处作访问或博士后研究。曾先后在武汉大学和中山大学的附属医院麻醉科及香港大学麻醉学系工作。主要从事心肌缺血再灌注损伤研究,在Anesthesiology、Cell Metabolism、Diabetes、Intensive Care Medicine、Critical Care Medicine、Free Radical Biology and Medicine、European Heart Journal及Circulation等发表SCI研究论文260余篇(3篇在Web of Science上高引),论文被引用26 220余次,H-index 60。曾主持8项香港研究资助局基金课题、1项国际心血管麻醉师学会课题、1项香港政府医疗卫生研究基金、1项香港AoE(卓越科学领域)分课题,另外主持6项国家自然科学基金课题。担任Lancet、Lancet Digit Health、Diabetes、Redox Biology、EClinicalMedicine等30多种学术期刊审稿人及加拿大、瑞士、克罗地亚、中国国家科研基金课题评审专家。发表的论文{XIA Z, HUANG Z, ANSLEY D M. Large-dose propofol during cardiopulmonary bypass decreases biochemical markers of myocardial injury in coronary surgery patients:a comparison with isoflurane. Anesth Analg, 6,3(3):527-53;2.}被2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery引用,推动了相关临床的实践与研究。2005年与加拿大David Ansley教授共同获得国际麻醉研究学会临床学者奖,2019年获得香港大学医学院杰出研究成果奖,并被国际著名医学评级机构(Expertscape)评为2011—2021糖尿病心肌病领域全球Top 1%(香港Top 1)专家、2012—2022实验糖尿病领域全球Top 0.1%专家(香港Top 1)。连续3年(2020─2022年)入选斯坦福全球2%顶尖科学家名单。获得广东省科技进步二等奖1项(2022年),湖北省科技进步二等奖1项(1998年);广东省卫健委“珠江人才计划”科技创新类领军人才(2022年);2023年全国麻醉医学领域学者学术影响力排名第一。

作者简介:

周嘉琪,硕士研究生,研究方向为糖尿病心肌病及心肌缺血再灌注损伤,E-mail:731252649@qq.com。

基金项目:

国家自然科学基金项目(82270306)


Targeting CD36 to regulate lipid metabolism:a new strategy for the prevention and treatment of diabetic cardiomyopathy
Author:
Affiliation:

1.Department of Anesthesiology, Affiliated Hospital of Guangdong Medical University, Zhanjian, Guangdong 524000, China;2.State Key Laboratory of Pharmaceutical Biotechnology, Department of Medicine, University of Hong Kong, Hong Kong 999077, China;3.Doctoral Training Platform for Research and Translation, Boshiwan, Guanchong Village, Zhongxiang, Hubei 431900, China)

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    摘要:

    脂质代谢异常诱发心肌结构和功能紊乱,进而导致糖尿病心肌病(DCM)的形成,已成为当前DCM研究的热点。CD36是主要的脂质跨膜转运蛋白,参与调节心脏脂质代谢,在DCM导致心肌损伤的分子机制中具有关键作用。本文总结了CD36的结构及其在特定细胞类型中的作用,并进一步探讨CD36在DCM中的病理生理作用,以及CD36作为靶点的潜在药物治疗策略。

    Abstract:

    Abnormalities in lipid metabolism induce myocardial structural and functional disorders, leading to the development of diabetic cardiomyopathy (DCM), which has become a hotspot in current DCM research. The transmembrane glycoprotein CD36 is a multifunctional membrane protein that facilitates fatty acid transport, which is involved in the regulation of cardiac lipid metabolism. CD36 signaling plays a key role in the pathogenesis of DCM mediated cardiac injuries. This article summarizes the structure of CD36 and its role in specific cell types, and further explores the pathophysiological role of CD36 in DCM, proposing that targeting CD36 may prove to be a potential pharmacological strategy in the prevention and treatment of DCM.

    参考文献
    [1] XIA W, LI X, WU Q, et al.The importance of caveolin as a target in the prevention and treatment of diabetic cardiomyopathy.Front Immunol, 2,3:951381.
    [2] GLATZ J F C, HEATHER L C, LUIKEN J.CD36 as a gatekeeper of myocardial lipid metabolism and therapeutic target for metabolic disease.Physiol Rev, 2023.DOI:10.1152/physrev.00011.2023.
    [3] UMBARAWAN Y, KAWAKAMI R, SYAMSUNARNO M, et al.Reduced fatty acid use from CD36 deficiency deteriorates streptozotocin-induced diabetic cardiomyopathy in mice.Metabolites, 1,1(12):881.
    [4] KUDA O, PIETKA T A, DEMIANOVA Z, et al.Sulfo-N-succinimidyl oleate (SSO) inhibits fatty acid uptake and signaling for intracellular calcium via binding CD36 lysine 164:SSO also inhibits oxidized low density lipoprotein uptake by macrophages.J Biol Chem, 3,8:15547-15555.
    [5] NECULAI D, SCHWAKE M, RAVICHANDRAN M, et al.Structure of LIMP-2 provides functional insights with implications for SR-BI and CD36.Nature, 3,4:172-176.
    [6] GILDE A J, VAN DER LEE K A, WILLEMSEN P H, et al.Peroxisome proliferator-activated receptor (PPAR) alpha and PPARbeta/delta, but not PPARgamma, modulate the expression of genes involved in cardiac lipid metabolism.Circ Res, 3,2:518-524.
    [7] SUGI K, HSIEH P N, ILKAYEVA O, et al.Kruppel-like factor 15 is required for the cardiac adaptive response to fasting.PLoS One, 8,3:e0192376.
    [8] SAMOVSKI D, SUN J, PIETKA T, et al.Regulation of AMPK activation by CD36 links fatty acid uptake to β-oxidation.Diabetes, 5,4:353-359.
    [9] GLATZ J F C, LUIKEN J.Dynamic role of the transmembrane glycoprotein CD36 (SR-B2) in cellular fatty acid uptake and utilization.J Lipid Res, 8,9:1084-1093.
    [10] SCHWENK R W, DIRKX E, COUMANS W A, et al.Requirement for distinct vesicle-associated membrane proteins in insulin-and AMP-activated protein kinase (AMPK)-induced translocation of GLUT4 and CD36 in cultured cardiomyocytes.Diabetologia, 0,3:2209-2219.
    [11] LIU Y, STEINBUSCH L K M, NABBEN M, et al.Palmitate-induced vacuolar-type H+-ATPase inhibition feeds forward into insulin resistance and contractile dysfunction.Diabetes, 7,6:1521-1534.
    [12] REN B, BEST B, RAMAKRISHNAN D P, et al.LPA/PKD-1-FoxO1 signaling axis mediates endothelial cell CD36 transcriptional repression and proangiogenic and proarteriogenic reprogramming.Arterioscler Thromb Vasc Biol, 6,6:1197-1208.
    [13] CHU L Y, RAMAKRISHNAN D P, SILVERSTEIN R L.Thrombospondin-1 modulates VEGF signaling via CD36 by recruiting SHP-1 to VEGFR2 complex in microvascular endothelial cells.Blood, 3,2:1822-1832.
    [14] BOU KHZAM L, SON N H, MULLICK A E, et al.Endothelial cell CD36 deficiency prevents normal angiogenesis and vascular repair.Am J Transl Res, 0,2:7737-7761.
    [15] GERBOD-GIANNONE M C, DALLET L, NAUDIN G, et al.Involvement of caveolin-1 and CD36 in native LDL endocytosis by endothelial cells.Biochim Biophys Acta Gen Subj, 9,3:830-838.
    [16] 蔡雅杰, 范晓迪, 白瑞娜.乳糜微粒在动脉粥样硬化防治中的作用.中国动脉硬化杂志, 3,1(9):799-805.CAI Y J, FAN X D, BAI R N.Role of coeliac particles in the prevention and treatment of atherosclerosis.Chin J Arterioscler, 3,1(9):799-805.
    [17] LI W, FEBBRAIO M, REDDY S P, et al.CD36 participates in a signaling pathway that regulates ROS formation in murine VSMCs.J Clin Invest, 0,0:3996-4006.
    [18] YANG M, SILVERSTEIN R L.CD36 signaling in vascular redox stress.Free Radic Biol Med, 9,6:159-171.
    [19] LI T T, CUI Y T, LI T H, et al.TM6SF2 reduces lipid accumulation in vascular smooth muscle cells by inhibiting LOX-1 and CD36 expression.Exp Cell Res, 3,9:113666.
    [20] YUE H, FEBBRAIO M, KLENOTIC P A, et al.CD36 enhances vascular smooth muscle cell proliferation and development of neointimal hyperplasia.Arterioscler Thromb Vasc Biol, 9,9:263-275.
    [21] VANHOUTTE D, SCHIPS T G, VO A, et al.Thbs1 induces lethal cardiac atrophy through PERK-ATF4 regulated autophagy.Nat Commun, 1,2:3928.
    [22] DELEON-PENNELL K Y, TIAN Y, ZHANG B, et al.CD36 is a matrix metalloproteinase-9 substrate that stimulates neutrophil apoptosis and removal during cardiac remodeling.Circ Cardiovasc Genet, 6,9:14-25.
    [23] IYER R P, PATTERSON N L, ZOUEIN F A, et al.Early matrix metalloproteinase-12 inhibition worsens post-myocardial infarction cardiac dysfunction by delaying inflammation resolution.Int J Cardiol, 5,5:198-208.
    [24] TANG Y, PAN B, ZHOU X, et al.Wip1-dependent modulation of macrophage migration and phagocytosis.Redox Biol, 7,3:665-673.
    [25] ZHANG X, XU H, YU J, et al.Immune regulation of the liver through the PCSK9/CD36 pathway during heart transplant rejection.Circulation, 3,8:336-353.
    [26] YANG J, SAMBANDAM N, HAN X, et al.CD36 deficiency rescues lipotoxic cardiomyopathy.Circ Res, 7,0:1208-1217.
    [27] CHISTIAKOV D A, OREKHOV A N, BOBRYSHEV Y V.The impact of FOXO-1 to cardiac pathology in diabetes mellitus and diabetes-related metabolic abnormalities.Int J Cardiol, 7,5:236-244.
    [28] ZHAN J, JIN K, DING N, et al.Positive feedback loop of miR-320 and CD36 regulates the hyperglycemic memory-induced diabetic diastolic cardiac dysfunction.Mol Ther Nucleic Acids, 3,1:122-138.
    [29] XU L, CHEN W, MA M, et al.Microarray profiling analysis identifies the mechanism of miR-200b-3p/mRNA-CD36 affecting diabetic cardiomyopathy via peroxisome proliferator activated receptor-γ signaling pathway.J Cell Biochem, 9,0:5193-5206.
    [30] MA X M, GENG K, LAW B Y, et al.Lipotoxicity-induced mtDNA release promotes diabetic cardiomyopathy by activating the cGAS-STING pathway in obesity-related diabetes.Cell Biol Toxicol, 3,9:277-299.
    [31] SCHULZE P C, DROSATOS K, GOLDBERG I J.Lipid use and misuse by the heart.Circ Res, 6,8:1736-1751.
    [32] PHAM T, LOISELLE D, POWER A, et al.Mitochondrial inefficiencies and anoxic ATP hydrolysis capacities in diabetic rat heart.Am J Physiol Cell Physiol, 4,7:C499-C507.
    [33] KUANG M, FEBBRAIO M, WAGG C, et al.Fatty acid translocase/CD36 deficiency does not energetically or functionally compromise hearts before or after ischemia.Circulation, 4,9:1550-1557.
    [34] LIN J, WANG T, LI Y, et al.N-acetylcysteine restores sevoflurane postconditioning cardioprotection against myocardial ischemia-reperfusion injury in diabetic rats.J Diabetes Res, 6,6:9213034.
    [35] MCBRIDE M R, MISTRETTA C M.Taste responses from the chorda tympani nerve in young and old Fischer rats.J Gerontol, 6,1:306-314.
    [36] WU L, WANG K, WANG W, et al.Glucagon-like peptide-1 ameliorates cardiac lipotoxicity in diabetic cardiomyopathy via the PPARα pathway.Aging Cell, 8,7:e12763.
    [37] JIN T, FU X, LIU M, et al.Finerenone attenuates myocardial apoptosis, metabolic disturbance and myocardial fibrosis in type 2 diabetes mellitus.Diabetol Metab Syndr, 3,5:87.
    [38] ZHAO T, CHEN H, CHENG C, et al.Liraglutide protects high-glucose-stimulated fibroblasts by activating the CD36-JNK-AP1 pathway to downregulate P4HA1.Biomed Pharmacother, 9,8:109224.
    [39] WANG Z, ZHU Y, ZHANG Y, et al.Protective effects of AS-Ⅳ on diabetic cardiomyopathy by improving myocardial lipid metabolism in rat models of T2DM.Biomed Pharmacother, 0,7:110081.
    [40] LI X, LI Z, DONG X, et al.Astragaloside Ⅳ attenuates myocardial dysfunction in diabetic cardiomyopathy rats through downregulation of CD36-mediated ferroptosis.Phytother Res, 3,7:3042-3056.
    [41] YAN M, LIU S, ZENG W, et al.The Chinese herbal medicine Fufang Zhenzhu Tiaozhi ameliorates diabetic cardiomyopathy by regulating cardiac abnormal lipid metabolism and mitochondrial dynamics in diabetic mice.Biomed Pharmacother, 3,4:114919.
    [42] ZHANG X, HAO Y.Beneficial effects of echinacoside on diabetic cardiomyopathy in diabetic Db/Db mice.Drug Des Devel Ther, 0,4:5575-5587.
    [43] WANG S, SCHIANCHI F, NEUMANN D, et al.Specific amino acid supplementation rescues the heart from lipid overload-induced insulin resistance and contractile dysfunction by targeting the endosomal mTOR-v-ATPase axis.Mol Metab, 1,3:101293.
    [44] RAMREZ E, PICATOSTE B, GONZLEZ-BRIS A, et al.Sitagliptin improved glucose assimilation in detriment of fatty-acid utilization in experimental type-II diabetes:role of GLP-1 isoforms in Glut4 receptor trafficking.Cardiovasc Diabetol, 8,7:12.
    [45] YING Y, ZHU H, LIANG Z, et al.GLP1 protects cardiomyocytes from palmitate-induced apoptosis via Akt/GSK3b/β-catenin pathway.J Mol Endocrinol, 5,5:245-262.
    [46] YU M, DU H, WANG B, et al.Exogenous H2S induces Hrd1 S-sulfhydration and prevents CD36 translocation via VAMP3 ubiquitylation in diabetic hearts.Aging Dis, 0,1:286-300.
    [47] SON N H, BASU D, SAMOVSKI D, et al.Endothelial cell CD36 optimizes tissue fatty acid uptake.J Clin Invest, 8,8:4329-4342.
    [48] LUIKEN J J, KOONEN D P, WILLEMS J, et al.Insulin stimulates long-chain fatty acid utilization by rat cardiac myocytes through cellular redistribution of FAT/CD36.Diabetes, 2,1:3113-3119.
    [49] JAY A G, SIMARD J R, HUANG N, et al.SSO and other putative inhibitors of FA transport across membranes by CD36 disrupt intracellular metabolism, but do not affect FA translocation.J Lipid Res, 0,1:790-807.
    [50] MANSOR L S, SOUSA FIALHO M D L, YEA G, et al.Inhibition of sarcolemmal FAT/CD36 by sulfo-N-succinimidyl oleate rapidly corrects metabolism and restores function in the diabetic heart following hypoxia/reoxygenation.Cardiovasc Res, 7,3:737-748.
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周嘉琪,林介夫,陈嘉佳,谢林,夏正远.靶向CD36调控脂质代谢:糖尿病心肌病防治新靶点[J].中国动脉硬化杂志,2023,31(12):1013~1019.

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  • 收稿日期:2023-11-16
  • 最后修改日期:2023-12-03
  • 在线发布日期: 2023-12-29