Inflammatory Links Between Hypertriglyceridemia and Atherogenesis.
Inflammatory Links Between Hypertriglyceridemia and Atherogenesis.
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DOI：
10.1007/s11883-022-01006-w
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发表时间：
2022-05
影响因子：
5.8
通讯作者：
Wu, Huaizhu
中科院分区：
文献类型：
--
作者：
Peng, Xueying;Wu, Huaizhu
关键词：
最近的研究表明，高甘油三酯血症（HTG）和动脉粥样硬化性心血管疾病（ASCVD）之间的关联。本综述的目的是讨论HTG和ASCVD风险之间的潜在机制以及HTG靶向治疗在ASCVD预防中的潜在疗效。HTG伴随富含甘油三酯的脂蛋白（TGRL）及其残余物升高，是ASCVD的致病风险因素。HTG增加ASCVD风险的机制尚不清楚，但可能包括多种因素。炎症在动脉粥样硬化中起着至关重要的作用。与低密度脂蛋白（LDL）相比，TGRL与炎症的相关性更好。TGRL残余物可穿透内皮并与巨噬细胞相互作用，导致动脉壁中的泡沫细胞形成和炎症，从而促进动脉粥样硬化形成。此外，循环单核细胞可以摄取TGRL并成为脂质负载的泡沫状单核细胞，其浸润动脉壁并也可能有助于动脉粥样硬化形成。针对HTG或炎症的新疗法正在开发中，并有可能降低与HTG相关的残留ASCVD风险。临床和临床前研究表明HTG在促进ASCVD中的因果作用，其中炎症起着至关重要的作用。针对HTG或炎症的新疗法有可能降低残余ASCVD风险。
Recent studies indicate an association between hypertriglyceridemia (HTG) and atherosclerotic cardiovascular disease (ASCVD). The purpose of this review is to discuss the potential mechanism connecting HTG and ASCVD risk and the potential efficacy of HTG-targeting therapies in ASCVD prevention. HTG, with elevations in triglyceride-rich lipoproteins (TGRL) and their remnants, are causal ASCVD risk factors. The mechanisms whereby HTG increases ASCVD risk are not well understood but may include multiple factors. Inflammation plays a crucial role in atherosclerosis. TGRL compared to low-density lipoproteins (LDL) correlate better with inflammation. TGRL remnants can penetrate endothelium and interact with macrophages leading to foam cell formation and inflammation in arterial walls, thereby contributing to atherogenesis. In addition, circulating monocytes can take up TGRL and become lipid-laden foamy monocytes, which infiltrate the arterial wall and may also contribute to atherogenesis. Novel therapies targeting HTG or inflammation are in development and have potential of reducing residual ASCVD risk associated with HTG. Clinical and preclinical studies show a causal role of HTG in promoting ASCVD, in which inflammation plays a vital role. Novel therapies targeting HTG or inflammation have potential of reducing residual ASCVD risk.
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影响因子：
39.3
作者：
Alexander, Veronica J.;Xia, Shuting;Tsimikas, Sotirios
通讯作者：
Tsimikas, Sotirios
脂质，糖尿病和冠心病的基因组关联研究信号的比较分析：心血管生物标志物遗传学协作。
影响因子：
39.3
作者：
Angelakopoulou A;Shah T;Sofat R;Shah S;Berry DJ;Cooper J;Palmen J;Tzoulaki I;Wong A;Jefferis BJ;Maniatis N;Drenos F;Gigante B;Hardy R;Laxton RC;Leander K;Motterle A;Simpson IA;Smeeth L;Thomson A;Verzilli C;Kuh D;Ireland H;Deanfield J;Caulfield M;Wallace C;Samani N;Munroe PB;Lathrop M;Fowkes FG;Marmot M;Whincup PH;Whittaker JC;de Faire U;Kivimaki M;Kumari M;Hypponen E;Power C;Humphries SE;Talmud PJ;Price J;Morris RW;Ye S;Casas JP;Hingorani AD
通讯作者：
Hingorani AD
影响因子：
30.8
作者：
Deloukas, Panos;Kanoni, Stavroula;Willenborg, Christina;Farrall, Martin;Assimes, Themistocles L.;Thompson, John R.;Ingelsson, Erik;Saleheen, Danish;Erdmann, Jeanette;Goldstein, Benjamin A.;Stirrups, Kathleen;Koenig, Inke R.;Cazier, Jean-Baptiste;Johansson, Asa;Hall, Alistair S.;Lee, Jong-Young;Willer, Cristen J.;Chambers, John C.;Esko, Tonu;Folkersen, Lasse;Goel, Anuj;Grundberg, Elin;Havulinna, Aki S.;Ho, Weang K.;Hopewell, Jemma C.;Eriksson, Niclas;Kleber, Marcus E.;Kristiansson, Kati;Lundmark, Per;Lyytikainen, Leo-Pekka;Rafelt, Suzanne;Shungin, Dmitry;Strawbridge, Rona J.;Thorleifsson, Gudmar;Tikkanen, Emmi;Van Zuydam, Natalie;Voight, Benjamin F.;Waite, Lindsay L.;Zhang, Weihua;Ziegler, Andreas;Absher, Devin;Altshuler, David;Balmforth, Anthony J.;Barroso, Ines;Braund, Peter S.;Burgdorf, Christof;Claudi-Boehm, Simone;Cox, David;Dimitriou, Maria;Do, Ron;Doney, Alex S. F.;El Mokhtari, NourEddine;Eriksson, Per;Fischer, Krista;Fontanillas, Pierre;Franco-Cereceda, Anders;Gigante, Bruna;Groop, Leif;Gustafsson, Stefan;Hager, Joerg;Hallmans, Goran;Han, Bok-Ghee;Hunt, Sarah E.;Kang, Hyun M.;Illig, Thomas;Kessler, Thorsten;Knowles, Joshua W.;Kolovou, Genovefa;Kuusisto, Johanna;Langenberg, Claudia;Langford, Cordelia;Leander, Karin;Lokki, Marja-Liisa;Lundmark, Anders;McCarthy, Mark I.;Meisinger, Christa;Melander, Olle;Mihailov, Evelin;Maouche, Seraya;Morris, Andrew D.;Mueller-Nurasyid, Martina;Nikus, Kjell;Peden, John F.;Rayner, N. William;Rasheed, Asif;Rosinger, Silke;Rubin, Diana;Rumpf, Moritz P.;Schaefer, Arne;Sivananthan, Mohan;Song, Ci;Stewart, Alexandre F. R.;Tan, Sian-Tsung;Thorgeirsson, Gudmundur;van der Schoot, C. Ellen;Wagner, Peter J.;Wells, George A.;Wild, Philipp S.;Yang, Tsun-Po;Amouyel, Philippe;Arveiler, Dominique;Basart, Hanneke;Boehnke, Michael;Boerwinkle, Eric;Brambilla, Paolo;Cambien, Francois;Cupples, Adrienne L.;de Faire, Ulf;Dehghan, Abbas;Diemert, Patrick;Epstein, Stephen E.;Evans, Alun;Ferrario, Marco M.;Ferrieres, Jean;Gauguier, Dominique;Go, Alan S.;Goodall, Alison H.;Gudnason, Villi;Hazen, Stanley L.;Holm, Hilma;Iribarren, Carlos;Jang, Yangsoo;Kahonen, Mika;Kee, Frank;Kim, Hyo-Soo;Klopp, Norman;Koenig, Wolfgang;Kratzer, Wolfgang;Kuulasmaa, Kari;Laakso, Markku;Laaksonen, Reijo;Lee, Ji-Young;Lind, Lars;Ouwehand, Willem H.;Parish, Sarah;Park, Jeong E.;Pedersen, Nancy L.;Peters, Annette;Quertermous, Thomas;Rader, Daniel J.;Salomaa, Veikko;Schadt, Eric;Shah, Svati H.;Sinisalo, Juha;Stark, Klaus;Stefansson, Kari;Tregouet, David-Alexandre;Virtamo, Jarmo;Wallentin, Lars;Wareham, Nicholas;Zimmermann, Martina E.;Nieminen, Markku S.;Hengstenberg, Christian;Sandhu, Manjinder S.;Pastinen, Tomi;Syvanen, Ann-Christine;Hovingh, G. Kees;Dedoussis, George;Franks, Paul W.;Lehtimaki, Terho;Metspalu, Andres;Zalloua, Pierre A.;Siegbahn, Agneta;Schreiber, Stefan;Ripatti, Samuli;Blankenberg, Stefan S.;Perola, Markus;Clarke, Robert;Boehm, Bernhard O.;O'Donnell, Christopher;Reilly, Muredach P.;Maerz, Winfried;Collins, Rory;Kathiresan, Sekar;Hamsten, Anders;Kooner, Jaspal S.;Thorsteinsdottir, Unnur;Danesh, John;Palmer, Colin N. A.;Roberts, Robert;Watkins, Hugh;Schunkert, Heribert;Samani, Nilesh J.
通讯作者：
Samani, Nilesh J.
影响因子：
7.7
作者：
Chait, Alan;Ginsberg, Henry N.;Bornfeldt, Karin E.
通讯作者：
Bornfeldt, Karin E.
影响因子：
5.3
作者：
Anderson, RA;Evans, ML;Frenneaux, MP
通讯作者：
Frenneaux, MP