[1]白斯特 潘建华 蔡梦珊 姜馨.白介素-1家族在急性冠状动脉综合征发生和发展过程中的机制及治疗现状进展[J].心血管病学进展,2022,(1):64-67.[doi:10.16806/j.cnki.issn.1004-3934.2022.01.017]
 BAI Site,PAN Jianhua,CAI Mengshan,et al.Mechanism and Treatment Status of Interleukin-1 Family in Occurrence and Development of Acute Coronary Syndrome[J].Advances in Cardiovascular Diseases,2022,(1):64-67.[doi:10.16806/j.cnki.issn.1004-3934.2022.01.017]
点击复制

白介素-1家族在急性冠状动脉综合征发生和发展过程中的机制及治疗现状进展()
分享到:

《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2022年1期
页码:
64-67
栏目:
出版日期:
2022-01-25

文章信息/Info

Title:
Mechanism and Treatment Status of Interleukin-1 Family in Occurrence and Development of Acute Coronary Syndrome
作者:
白斯特1 潘建华2 蔡梦珊1 姜馨3
(1.西安医学院,陕西 西安710068;2.陕西省康复医院影像科,陕西 西安 710065;3.陕西省人民医院心血管内科,陕西 西安710068)
Author(s):
BAI Site1 PAN Jianhua2 CAI Mengshan1 JIANG Xin3
(1.Xi’an Medical University,Xi’an 710068,Shaanxi,China; 2.Department of Radiology,Shaanxi Kangfu Hospital,Xi’an 710065,Shaanxi,China; 3.Department of Cardiovascular Medicine,Shaanxi Provincial Peoples Hospital,Xi’an 710068,Shaanxi,China)
关键词:
白介素-1急性冠状动脉综合征细胞因子炎症
Keywords:
Interleukin-1Acute coronary syndromeCytokinesInflammatory
DOI:
10.16806/j.cnki.issn.1004-3934.2022.01.017
摘要:
白介素(IL)-1家族是一类发现较早且作用广泛的炎症细胞因子,在急性冠状动脉综合征的发生和发展过程中发挥着至关重要的作用。IL-1家族成员包括IL-1α、IL-1β、IL-1Ra、IL-18、IL-33、IL-36α、IL-36β、IL-36γ、IL-36Ra、IL-37和IL-38。它们在急性冠状动脉综合征的发生和发展过程中展现出各自的抗炎及促炎作用。目前已有研究探索将其用于急性冠状动脉综合征的治疗并取得良好效果。现对IL-1家族参与急性冠状动脉综合征发生和发展的机制及治疗现状进行综述。
Abstract:
Interleukin (IL) - 1 family is a kind of inflammatory cytokines found earlier and widely used. It plays an important role in the occurrence and development of acute coronary syndrome. Members of the IL-1 family include IL-1α,IL-1β,IL-1Ra,IL-18,IL-33,IL-36α,IL-36β,IL-36γ,IL-36Ra,IL-37,and IL-38. They respectively exhibit anti-inflammatory and pro-inflammatory effects in the development of acute coronary syndrome. At present,studies have explored its use in the treatment of acute coronary syndrome and achieved good results. This paper reviews the mechanism and treatment status of IL-1 family involved in the occurrence and development of acute coronary syndrome.

参考文献/References:

[1] GBD 2019 Diseases and Injuries Collaborators. Global burden of 369 diseases and injuries in 204 countries and territories,1990—2019:a systematic analysis for the Global Burden of Disease Study 2019[J]. Lancet,2020,396(10258):1204-1222.

[2] 国家卫生计生委合理用药专家委员会,中国药师协会. 冠心病合理用药指南(第2版)[J].中国医学前沿杂志(电子版),2018,10(6):1-130.

[3] Waterbury TM,Tarantini G,Vogel B,et al. Non-atherosclerotic causes of acute coronary syndromes[J]. Nat Rev Cardiol,2020,17(4):229-241.

[4] Hedin U,Matic LP. Recent advances in therapeutic targeting of inflammation in atherosclerosis[J]. J Vasc Surg,2019,69(3):944-951.

[5] Silvestre-Roig C,Braster Q,Ortega-Gomez A,et al. Neutrophils as regulators of cardiovascular inflammation[J]. Nat Rev Cardiol,2020,17(6):327-340.

[6] Mantovani A,Dinarello CA,Molgora M,et al. Interleukin-1 and related cytokines in the regulation of inflammation and immunity[J]. Immunity,2019,50(4):778-795.

[7] Migliorini P,Italiani P,Pratesi F,et al. The IL-1 family cytokines and receptors in autoimmune diseases[J]. Autoimmun Rev,2020,19(9):102617.

[8] Cavalli G,Colafrancesco S,Emmi G,et al. Interleukin 1α:a comprehensive review on the role of IL-1α in the pathogenesis and treatment of autoimmune and inflammatory diseases[J]. Autoimmun Rev,2021,20(3):102763.

[9] Suzuki K,Murtuza B,Smolenski RT,et al. Overexpression of interleukin-1 receptor antagonist provides cardioprotection against ischemia-reperfusion injury associated with reduction in apoptosis[J]. Circulation,2001,104(12 suppl 1):I308-I313.

[10] Furuichi K,Wada T,Iwata Y,et al. Interleukin-1-dependent sequential chemokine expression and inflammatory cell infiltration in ischemia-reperfusion injury[J]. Crit Care Med,2006,34 (9):2447-2455.

[11] Pinteaux E,Rothwell NJ,Boutin H. Neuroprotective actions of endogenous interleukin-1 receptor antagonist(IL-1ra) are mediated by glia[J]. Glia,2006,53(5):551-556.

[12] Bujak M,Dobaczewski M,Chatila K,et al. Interleukin-1 receptor typeⅠsignaling critically regulates infarct healing and cardiac remodeling[J]. Am J Pathol,2008,173(1):57-67.

[13] Mauro AG,Mezzaroma E,Torrado J,et al. Reduction of myocardial ischemia-reperfusion injury by inhibiting interleukin-1 alpha[J]. J Cardiovasc Pharmacol,2017,69(3):156-160.

[14] The Interleukin 1 Genetics Consortium. Cardiometabolic effects of genetic upregulation of the interleukin 1 receptor antagonist:a Mendelian randomisation analysis[J]. Lancet Diabetes Endocrinol,2015,3(4):243-253.

[15] Abbate A,van Tassell BW,Biondi-Zoccai G,et al. Effects of interleukin-1 blockade with anakinra on adverse cardiac remodeling and heart failure after acute myocardial infarction [from the Virginia Commonwealth University-Anakinra Remodeling Trial (2) (VCU-ART2) pilot study][J]. Am J Cardiol,2013,111(10):1394-1400.

[16] Abbate A,Kontos MC,Grizzard JD,et al. Interleukin-1 blockade with anakinra to prevent adverse cardiac remodeling after acute myocardial infarction(Virginia Commonwealth University Anakinra Remodeling Trial[VCU-ART] Pilot study)[J]. Am J Cardiol,2010,105(10):1371-1377.e1.

[17] Morton AC,Rothman AMK,Greenwood JP,et al. The effect of interleukin-1 receptor antagonist therapy on markers of inflammation in non-ST elevation acute coronary syndromes:the MRC-ILA Heart Study[J]. Eur Heart J,2015,36(6):377-384.

[18] Dinarello CA. Overview of the IL-1 family in innate inflammation and acquired immunity[J]. Immunol Rev,2018,281(1):8-27.

[19] Kim B,Lee Y,Kim E,et al. The interleukin-1α precursor is biologically active and is likely a key alarmin in the IL-1 family of cytokines[J]. Front Immunol,2013,4:391.

[20] Libby P. Interleukin-1 beta as a target for atherosclerosis therapy:biological basis of CANTOS and beyond[J]. J Am Coll Cardiol,2017,70(18):2278-2289.

[21] Tong Y,Wang Z,Cai L,et al. NLRP3 inflammasome and its central role in the cardiovascular diseases[J]. Oxid Med Cell Longev,2020,2020:4293206.

[22] Shikama Y,Aki N,Hata A,et al. Palmitate-stimulated monocytes induce adhesion molecule expression in endothelial cells via IL-1 signaling pathway[J]. J Cell Physiol,2015,230(3):732-742.

[23] Ridker PM,Everett BM,Thuren T,et al. Antiinflammatory therapy with canakinumab for atherosclerotic disease[J]. N Eng J Med,2017,377(12):1119-1131.

[24] Ridker PM,MacFadyen JG,Thuren T,et al. Residual inflammatory risk associated with interleukin-18 and interleukin-6 after successful interleukin-1β inhibition with canakinumab:further rationale for the development of targeted anti-cytokine therapies for the treatment of atherothrombosis[J]. Eur Heart J,2020,41(23):2153-2163.

[25] Novick D,Kim S,Kaplanski G,et al. Interleukin-18,more than a Th1 cytokine[J]. Semin Immunol,2013,25(6):439-448.

[26] Kaptoge S,Seshasai SR,Gao P,et al. Inflammatory cytokines and risk of coronary heart disease:new prospective study and updated meta-analysis[J]. Eur Heart J,2014,35(9):578-589.

[27] ?kerblom A,James SK,Lakic TG,et al. Interleukin-18 in patients with acute coronary syndromes[J]. Clin Cardiol,2019,42(12):1202-1209.

[28] Dinarello CA. The IL-1 family of cytokines and receptors in rheumatic diseases[J]. Nat Rev Rheumatol,2019,15(10):612-632.

[29] Cayrol C,Girard JP. Interleukin-33(IL-33):a nuclear cytokine from the IL-1 family[J] . Immunol Rev,2018,281(1):154-168.

[30] Bertheloot D,Latz E. HMGB1,IL-1α,IL-33 and S100 proteins:dual-function alarmins[J]. Cell Mol Immunol,2017,14(1):43-64.

[31] Gurgone D,McShane L,McSharry C,et al. Cytokines at the interplay between asthma and atherosclerosis?[J]. Front Pharmacol,2020,11:166.

[32] Miller AM,Xu D,Asquith DL,et al. IL-33 reduces the development of atherosclerosis[J]. J Exp Med,2008,205(2):339-346.

[33] Martin P,Palmer G,Rodriguez E,et al. Atherosclerosis severity is not affected by a deficiency in IL-33/ST2 signaling[J]. Immun Inflamm Dis,2015,3(3):239-246.

[34] Liu CL,Shen DL,Zhu K,et al. Characterization of interleukin-33 and matrix metalloproteinase-28 in serum and their association with disease severity in patients with coronary heart disease[J]. Coron Artery Dis,2014,25(6):498-504.

[35] Al Shahi H,Shimada K,Miyauchi K,et al. Elevated circulating levels of inflammatory markers in patients with acute coronary syndrome[J]. Int J Vasc Med,2015,2015:805375.

[36] Demyanets S,Speidl WS,Tentzeris I,et al. Soluble ST2 and interleukin-33 levels in coronary artery disease:relation to disease activity and adverse outcome[J]. PLoS One,2014,9(4):e95055.

[37] Han Y,Huard A,Mora J,et al. IL-36 family cytokines in protective versus destructive inflammation[J]. Cell Signal,2020,75:109773.

[38] Tian Y,Ling XY,Chen DL,et al. Interleukin-36 receptor antagonist attenuates atherosclerosis development by inhibiting NLRP3 inflammasome[J]. J Cell Physiol,2020,235(12):9992-9996.

[39] Jia H,Liu J,Han B. Reviews of interleukin-37:functions,receptors,and roles in diseases[J]. Biomed Res Int,2018,2018:3058640.

[40] Li H,Shen C,Chen B,et al. Interleukin-37 is increased in peripheral blood mononuclear cells of coronary heart disease patients and inhibits the inflammatory reaction[J]. Mol Med Rep,2020,21(1):151-160.

[41] Lotfy H,Moaaz M,Moaaz M. The novel role of IL-37 to enhance the anti-inflammatory response of regulatory T cells in patients with peripheral atherosclerosis[J]. Vascular,2020,28(5):629-642.

[42] Zhong Y,Yu K,Wang X,et al. Elevated plasma IL-38 concentrations in patients with acute ST-segment elevation myocardial infarction and their dynamics after reperfusion treatment[J]. Mediators Inflamm,2015,2015:490120.

[43] Wei Y,Lan Y,Zhong Y,et al. Interleukin-38 alleviates cardiac remodelling after myocardial infarction[J]. J Cell Mol Med,2020,24(1):371-384.

相似文献/References:

[1]韩雅君,朱慧,王丽媛,等.虚拟组织学对急性冠状动脉综合征患者斑块评价研究进展[J].心血管病学进展,2015,(5):641.[doi:10.3969/j.issn.1004-3934.2015.05.031]
 HAN Yajun,ZHU Hui,WANG Liyuan,et al.Evaluating Plaque in Patients with Acute Coronary Syndrome by Intravascular Ultrasound with Virtual Histology[J].Advances in Cardiovascular Diseases,2015,(1):641.[doi:10.3969/j.issn.1004-3934.2015.05.031]
[2]郭远林.急性冠状动脉综合征风险评估方法学进展[J].心血管病学进展,2015,(6):681.[doi:10.3969/j.issn.1004-3934.2015.06.007]
 GUO Yuanlin,YAN Hongbin.Progress in Tools for Risk Assessment of Acute Coronary Syndromes[J].Advances in Cardiovascular Diseases,2015,(1):681.[doi:10.3969/j.issn.1004-3934.2015.06.007]
[3]魏恒争,木胡牙提.比伐卢定在急性冠状动脉综合征患者PCI中的应用进展[J].心血管病学进展,2015,(6):725.[doi:10.3969/j.issn.1004-3934.2015.06.017]
 WEI Hengzheng,MUHU Yati.Advance in Research of Bivalirudin During Percutaneous Coronary Intervention in Patients with Acute Coronary Syndrome[J].Advances in Cardiovascular Diseases,2015,(1):725.[doi:10.3969/j.issn.1004-3934.2015.06.017]
[4]丁晓彤 张欣 左海奇 孙雨萌 贾赫 刘宏伟 孙鑫 孙延明 王岚峰 王姝.应激性心肌病诊治进展[J].心血管病学进展,2019,(5):778.[doi:10.16806/j.cnki.issn.1004-3934. 2019.05.028]
 DING Xiaotong,ZHANG Xin,ZUO Haiqi,et al.Diagnosis and Treatment of Takotsubo Sydrome[J].Advances in Cardiovascular Diseases,2019,(1):778.[doi:10.16806/j.cnki.issn.1004-3934. 2019.05.028]
[5]陈纪元 陆泓雨 贺子熠 韩江莉.冠心病合并慢性肾脏病患者P2Y12受体拮抗剂治疗进展[J].心血管病学进展,2022,(7):582.[doi:10.16806/j.cnki.issn.1004-3934.2022.07.000]
 CHEN Jiyuan,LU Hongyu,HE Ziyi,et al.P2Y12 Antagonists for Patients with Chronic Kidney Diseases and Coronary Heart Diseases[J].Advances in Cardiovascular Diseases,2022,(1):582.[doi:10.16806/j.cnki.issn.1004-3934.2022.07.000]

备注/Memo

备注/Memo:
收稿日期:2021-06-04
更新日期/Last Update: 2022-02-17