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Role of chronic endoplasmic reticulum stress induced apoptosis in atherosclerotic plaque formation
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1. College of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210046, China;2. College of Chemical Engineering, Huaiyin Institute of Technology, Huai’an, Jiangsu 223003, China;3. Jiangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica, School of Pharmacy, Nanjing, Jiangsu 210046, China )

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R363

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    Abstract:

    The endoplasmic reticulum stress(ERS) has emerged as a factor that is relevant to a number of systemic and arterial-wall factors that promote atherosclerosis(As). Prolonged activation of ERS pathway known as the unfolded protein response (UPR) can lead to cell pathology and subsequent tissue dysfunction. There is now ample evidence that the UPR is chronically activated in atherosclerotic lesional cells, particularly advanced lesional macrophages and endothelial cells. The stressors in advanced lesions that can lead to prolonged activation of the UPR include oxidative stress, oxysterols, and high levels of intracellular cholesterol and saturated fatty acids. These arterial-wall stressors may be especially prominent in the settings of obesity, insulin resistance, and diabetes, all of which promote the clinical progression of As. While exciting work over the last decade has begun to shed light on the mechanisms and in vivo relevance of ERS-driven As, much more work is needed to fully understand this area and to enable an informed approach to therapeutic translation.

    Reference
    [1] 伍熙, 赵东晖, 范谦, 等.成纤维细胞生长因子21对载脂蛋白E基因敲除小鼠动脉粥样硬化病变中内质网应激诱导的凋亡的影响.中国动脉硬化杂志, 4,2(4): 325-329.
    [2] 马亚红, 唐寅, 阿布杜拉·热西提, 等.载脂蛋白CⅢ通过增加氧化应激及内质网应激水平促进动脉粥样硬化病变.中国动脉硬化杂志, 6,4(2): 135-140.
    [3] Myoishi M, Hao H, Kitakaze M.Increased endoplasmic reticulum stress in atherosclerotic plaques associated with acute coronary syndromes.J Mol Cell Cardiol, 7,6(11): 1 226-233.
    [4] Schrijvers DM.Phagocytosis in atherosclerosis: Molecular mechanisms and implications for plaque progression and stability.Cardiov Res, 7,3(3): 470-480.
    [5] Thorp E, Li G, Seimon TA, et al.Reduced apoptosis and plaque necrosis in advanced atherosclerotic lesions of Apoe-/- and Ldlr-/- mice lacking CHOP.Cell Metab, 9,9(5): 474-481.
    [6] Oyadomari S, Mori M.Roles of CHOP/GADD153 in endoplasmic reticulum stress.Cell Death Differ, 4,1(4): 381-389.
    [7] Dmitry AC, Igor AS, Alexander NO, et al.Role of endoplasmic reticulum stress in atherosclerosis and diabetic macrovascular complications.Biomed Res Int, 4,4(3):610 140.
    [8] Tabas I, Garcíacardea G, Owens GK.The cell biology of disease:recent insights into the cellular biology of atherosclerosis.J Cell Biol, 5,9(1): 13.
    [9] Adzhemian NA, Kiseleva TN, Ezhov MV, et al.Changes of ocular blood flow in patients with subclinical atherosclerosis.Atherosclerosis, 5,1(1): e160.
    [10] Beraia M, Beraia G.Investigation of the blood flow at the boundary layer by the magnetic resonance angiography in atherosclerosis.Atherosclerosis, 4,5(2): e156.
    [11] Civelek M, Manduchi E, Riley RJ, et al.Chronic endoplasmic reticulum stress activates unfolded protein response in arterial endothelium in regions of susceptibility to atherosclerosis.Circ Res, 9,5(5): 453-461.
    [12] Tabas I, Garcíacardea G, Owens GK.Recent insights into the cellular biology of atherosclerosis.J Cell Biol, 5,9(1): 13-22.
    [13] Martin D, Li Y, Yang J, et al.Unspliced X-box-binding protein 1 (xbp1) protects endothelial cells from oxidative stress through interaction with histone deacetylase 3.J Biol Chem, 4,9(44): 30 625-634.
    [14] Lipskaia L, Keuylian Z, Blirando K, et al.Expression of sarco (endo) plasmic reticulum calcium ATPase (SERCA) system in normal mouse cardiovascular tissues, heart failure and atherosclerosis.BBA Biomem, 4,3(11): 2 705-718.
    [15] Suhara T, Fukuo K, Yasuda O, et al.Homocysteine enhances endothelial apoptosis via upregulation of Fas-mediated pathways.Hypertension, 4,3(6): 1 208-213.
    [16] Zulli A, Lau E, Wijaya BPP, et al.High dietary taurine reduces apoptosis and atherosclerosis in the left main coronary artery: association with reduced CCAAT/enhancer binding protein homologous protein and total plasma homocysteine but not lipidemia.Hypertension, 9,3(6): 1 017-022.
    [17] Tabas I, Seimon T, Timmins J, et al.Macrophage apoptosis in advanced atherosclerosis.Ann Ny Acad Sci, 9,3(s1): E40-E45.
    [18] 滕林, 杨伟, 周飞, 等.内质网应激蛋白CHOP-10在缺血缺氧诱导人主动脉内皮细胞损伤中的作用.中国动脉硬化杂志, 6,4(3): 245-250.
    [19] Lin JH, Li H, Yasumura D, et al.IRE1 signaling affects cell fate during the unfolded protein response.Science, 7,8(5852): 944-949.
    [20] Sanson M, Augé N, Vindis C, et al.Oxidized low-density lipoproteins trigger endoplasmic reticulum stress in vascular cells: prevention by oxygen-regulated protein 150 expression.Circ Res, 9,4(3): 328-336.
    [21] Dickhout JG, Colgan SM, Sárka L, et al.Increased endoplasmic reticulum stress in atherosclerotic plaques associated with acute coronary syndrome: a balancing act between plaque stability and rupture.J Mol Cell Cardiol, 6,1(6): 1 226-233.
    [22] Myoishi M, Hao H, Kitakaze M.Increased endoplasmic reticulum stress in atherosclerotic plaques associate奤??婩桴慨渠条?????楣慯湲杯????攠瑳?慮汤?副敭摥畳挮瑊椠潍湯?漠晃???倠?慡捲瑤楩癯慬琬攠搷?瀶爨漱琱攩椺渠?欠椲渱愴猭攲?愶氮瀼桢慲￣??椊湛挲爳敝愠獒敡獯?敊測搠潚灨污慮獧洠楃挬?牗敡瑮楧挠畐氬甠浥?猠瑡牬攮獃猯?慂湐搠?慯瑭桯敬牯潧獯捵汳攠牰潲獯楴獥?楮渠?癃楈癏潐??楣牯据畴汲慩瑢極潴湥????ㄠ??????????戠牤????嬠??嵡??潨汥琠数湲楯?卯乴???愠獯獦椠潅?????楳物楧潮污潬??剧??敮琠?慣汵??氠畬瑩慶瑥桲椠潦湡敩?汵楲浥椮瑂獩??牨潥??摊攬瀠攴測搶攨渲琩?漠砳椶搹愭琳椷漸渮?楢湲￣琊栊攊?攲渴摝漠灊汩慮猠浈楏挬?牌敥瑥椠捙畈氬甠浐????楊潁氬??桴攠浡???????????????????????扳爠????嬠??嵡??氠慴楨獲??????桏楓渭??呤??婴楥瑤漠????攠瑡?慴汩???獩浯慮氠污?浤漠汰敯捴略汮整?楡湴桥楳戠楔瑒潁牉?漭晩?敤湵摣潥灤氠慣獥浬楬挠?牥敡瑴楨挠畩汮甠浢?潥硡楳摴愠瑣楡潮湣????敥牬潬???眠楃瑡桮?獥敲氠敒捥瑳椠癃敬汩祮?爠攴瘬攰爨猱椲戩氺攠′琠栰椳漹氭‰爴收愮挼瑢楲瘾椊琊礊??‵?椠潇污??案攬洠??と????????金ぃ???????ち????扏牐????孤??崳??慩湳?卡???楧慡湴杩??倠???敵癬牡楴敯獲?卯敦椠浌潐湓?呩??敵瑣?慤氠??愭挶爠潥灸桰慲来敳?楩湯獮甠汩楮渠?爠散捥敬灬瑳漮牍?摬攠晉業捭極敮湯捬礬?椹測挷爨攲愭猳攩猺??刹‰猭琳爹攷献猼?楲渾搊甊挊敛搲?慝瀠潃灬瑡潲獫楥猠?慃測搠?湩敧捧爠潎琬椠捍?捧潵物敲?映潊牊洬愠瑥楴漠湡?椮湁?慯摰癴慯湳捩敳搠?慦琠桶敡牳潣獵捬污敲爠潳瑭楯捯?汨攠獭極潳湣獬??散汥汬??攠瑩慮扤???????????????????扡牱????孵??嵥??湢潩灬?????潮甠晡整汨汥敲????噥敲汯汳潩獳漮?????湥摤漬瀠氶愬猲洨椹挩?爠攱琠椰挷电氭田洸‰献琼牢敲猾猊??潛戲攷獝椠瑚票?慵渠摊?摁楳慳扯散瑩敡獴?呯牮攠湯摦猠??潬汴??敬摥?????????????????扰牡????孹??嵷??楨愠湡杣??偬???慴湥?匠???楥????敬瑥?慯汳??洠灩慮椠牨敹摰?????獯楣杹湳慴汥楩湮来?慩湣搠?印?剬???数硲灯牴敥獩獮椠潅渭?灥牦潩浣潩瑥敮?攠牭?獣瑥爮敃獩獲?慵湬摡?慩灯潮瀬琠漴猬椰猨′椩渺?椲渰猷甭氲椱渳?爼敢獲椾猊琊愊湛琲?浝愠捋牥潤灩栠慘本攠獍?慮湧搠?愬爠教?牮敧癰敩牮獧攠摗?戠祥?攠硡敬渮慆瑲楥摥攠?瑨牯敬慥瑳浴敥湲瑯??楯慶扥敲瑬敯獡????ㄠ??つ??????ね???????扳牣????孥??嵳?呤慥扡慴獨???呤栠敡?牴潩汶敡?潥晤?敢湯摴潨瀠汅慒猭洠楡据?爠敭瑩楴捯畣汨畯浮?獲瑩牡敬猭獤?楰湥?瑤桥敮?瀠牤潥条牴敨猠獰楡潴湨?潡晹?慁瑴桨敥牲潯獳捣汬敥牲潯獳楩獳??椹爬挷?刱攩猺????????????????せ??扝爠????孴?っ嵫??楈????卡据甠汍汉????佭穩捡愠湇????攠瑡?愮汇?乵??偳??潩确楥搭慩獮敤?汣楥湤欠獥?敤湯摰潬灡汳慭獩浣椠捲?牴敩瑣極捬畵汭甠浤?獳瑦牵敮獣獴??潮砠楩摳愠瑡楳癳敯?獩瑡牴敥獤猠??慴湨搠?偣?剥?慥捲瑡楴癥慤琠楡潴湨?瑲潯?楣湬摥畲捯敳?慳瀠潩灮琠潡猠楨獹????敬汹汣??楩潣氠?????????????????????戠父????嬩?ㄠ崹″?愼灢潲甾氊愊搊敛″到???桨慥湮?????夠效慵湮杧????攠瑗?慮汧?佂硗椬搠楥穴攠摡?瀮桔潨獥瀠桭潯汬楥灣極摬獡??汲楥灧潵灬牡潴瑩敯楮渠?慦???慄湄搱‵瀳爠潩杮爠敡獰獯楰潴湯?潩晳?捯慦氠捣極晬楴捵?慥潤爠瑶楡捳?癵慬污癲攠?獭瑯敯湴潨猠業獵????洠??潬汬汳??慹爠摣楹潣汬?????????????㈠????????扃牡????孶??嵣??潥楳欬攠?听???椩愺渠朵‵??‵圵愹渮朼?塲??攊琊?愳氱??湊桩慡渠捆攬搠?慵漠牃琬椠捃?慥瑮栠敚爬漠獥捴氠敡牬漮獁楴獯?楶湡?瑴牡慴湩獮朠敩湮楨捩?睩慴瑳愠湨慯扭敯?桹敳牴楥瑩慮扥氭敩?桤祵灣敥牤氠楥灮楤摯数浬楡捳?物慣戠扲楥瑴獩?敵硬灵牭攠獳獴楲湥杳?氠楴灨潲灯牵潧瑨攠楡湣?汩楶灡慴獩敯??慯牦搠楁潍癐愭獡捣?剩敶獡???????????㈠???????扃牡????孶??嵣?婔桨略?堬?′匬琰攨父朩椺漠瀳漱男氭漳猲‵???坲甾?匊?剛椳猲歝?潌晥?栠祅灋攬爠瑊敥湯獮楧漠湊?愬渠摃?牡敮湧愠汊?搬礠獥晴甠湡捬琮楁潣湴?睶楡瑴桩?慮渠?慦渠杁楍潐札敡湣整獩楶獡?楥湤栠楰扲楯瑴潥物?猠畫湩楮瑡楳湥椠扩??獩祢獩瑴敳洠慡瑬楢捵?物敮瘭楩敮睤?慣湥摤?浥敮瑤慯?慬湡慳汭祩獣椠獲??捩瑣慵?併湭挠潳汴????????????????扩牳????扯牵?h inhibition of reactive oxygen species.Nephron Exp Nephrol, 2,1(1-2): e38-48.
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JING Yi, CAI Dan-Feng, LIN Chao, SUN Xin, BIAN Hui-Min. Role of chronic endoplasmic reticulum stress induced apoptosis in atherosclerotic plaque formation[J]. Editorial Office of Chinese Journal of Arteriosclerosis,2017,25(9):957-962.

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  • Received:December 01,2016
  • Revised:February 27,2017
  • Online: September 29,2017
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