Targeting Inflammatory Pathways in Cardiovascular Disease: The Inflammasome, Interleukin-1, Interleukin-6 and Beyond.
Targeting Inflammatory Pathways in Cardiovascular Disease: The Inflammasome, Interleukin-1, Interleukin-6 and Beyond.
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DOI：
10.3390/cells10040951
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发表时间：
2021-04-20
期刊：
影响因子：
6
通讯作者：
Libby P
中科院分区：
文献类型：
--
作者：
Libby P
最近的临床试验已经确定炎症参与了人类动脉粥样硬化的因果关系。这些观察结果为新的治疗方法指明了方向，这些新的治疗方法可以添加到现有的治疗方法中，以帮助阻止日益增长的全球心血管疾病流行。幸运的是，我们现在有许多可操作的目标，其临床探索将有助于实现优化有益效果的目标，同时避免对宿主防御或其他不必要的行为的不当干扰。本综述旨在通过对临床应用范围内抗炎干预措施的现状进行批判性评价，为这种探索提供基础，主要关注先天免疫。特别是，本文强调了从炎性小体，通过白细胞介素（IL）-1到IL-6的途径，这些途径得到了临床前，临床和人类遗传数据的支持。本文还考虑使用生物标志物来指导抗炎治疗的分配，作为实现精准医学承诺的一步。最近的临床研究验证了数十年的人类实验工作和相关研究，为进一步努力靶向动脉粥样硬化中的炎症提供了强大的动力，以解决尽管有当前的治疗方法，但仍然存在的相当大的风险。
Recent clinical trials have now firmly established that inflammation participates causally in human atherosclerosis. These observations point the way toward novel treatments that add to established therapies to help stem the growing global epidemic of cardiovascular disease. Fortunately, we now have a number of actionable targets whose clinical exploration will help achieve the goal of optimizing beneficial effects while avoiding undue interference with host defenses or other unwanted actions. This review aims to furnish the foundation for this quest by critical evaluation of the current state of anti-inflammatory interventions within close reach of clinical application, with a primary focus on innate immunity. In particular, this paper highlights the pathway from the inflammasome, through interleukin (IL)-1 to IL-6 supported by a promising body of pre-clinical, clinical, and human genetic data. This paper also considers the use of biomarkers to guide allocation of anti-inflammatory therapies as a step toward realizing the promise of precision medicine. The validation of decades of experimental work and association studies in humans by recent clinical investigations provides a strong impetus for further efforts to target inflammation in atherosclerosis to address the considerable risk that remains despite current therapies.
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影响因子：
64.8
作者：
Bick AG;Weinstock JS;Nandakumar SK;Fulco CP;Bao EL;Zekavat SM;Szeto MD;Liao X;Leventhal MJ;Nasser J;Chang K;Laurie C;Burugula BB;Gibson CJ;Lin AE;Taub MA;Aguet F;Ardlie K;Mitchell BD;Barnes KC;Moscati A;Fornage M;Redline S;Psaty BM;Silverman EK;Weiss ST;Palmer ND;Vasan RS;Burchard EG;Kardia SLR;He J;Kaplan RC;Smith NL;Arnett DK;Schwartz DA;Correa A;de Andrade M;Guo X;Konkle BA;Custer B;Peralta JM;Gui H;Meyers DA;McGarvey ST;Chen IY;Shoemaker MB;Peyser PA;Broome JG;Gogarten SM;Wang FF;Wong Q;Montasser ME;Daya M;Kenny EE;North KE;Launer LJ;Cade BE;Bis JC;Cho MH;Lasky-Su J;Bowden DW;Cupples LA;Mak ACY;Becker LC;Smith JA;Kelly TN;Aslibekyan S;Heckbert SR;Tiwari HK;Yang IV;Heit JA;Lubitz SA;Johnsen JM;Curran JE;Wenzel SE;Weeks DE;Rao DC;Darbar D;Moon JY;Tracy RP;Buth EJ;Rafaels N;Loos RJF;Durda P;Liu Y;Hou L;Lee J;Kachroo P;Freedman BI;Levy D;Bielak LF;Hixson JE;Floyd JS;Whitsel EA;Ellinor PT;Irvin MR;Fingerlin TE;Raffield LM;Armasu SM;Wheeler MM;Sabino EC;Blangero J;Williams LK;Levy BD;Sheu WH;Roden DM;Boerwinkle E;Manson JE;Mathias RA;Desai P;Taylor KD;Johnson AD;NHLBI Trans-Omics for Precision Medicine Consortium;Auer PL;Kooperberg C;Laurie CC;Blackwell TW;Smith AV;Zhao H;Lange E;Lange L;Rich SS;Rotter JI;Wilson JG;Scheet P;Kitzman JO;Lander ES;Engreitz JM;Ebert BL;Reiner AP;Jaiswal S;Abecasis G;Sankaran VG;Kathiresan S;Natarajan P
通讯作者：
Natarajan P
白介素-1和炎性体作为心血管疾病的治疗靶标。
影响因子：
20.1
作者：
Abbate A;Toldo S;Marchetti C;Kron J;Van Tassell BW;Dinarello CA
通讯作者：
Dinarello CA
影响因子：
5.6
作者：
Cavalli G;Dinarello CA
通讯作者：
Dinarello CA
影响因子：
37.8
作者：
Bick, Alexander G.;Pirruccello, James P.;Natarajan, Pradeep
通讯作者：
Natarajan, Pradeep
影响因子：
37.8
作者：
Biasucci, LM;Liuzzo, G;Maseri, A
通讯作者：
Maseri, A