[1]韩冰 来春林.黑色素瘤缺乏因子2炎症小体在心血管疾病中的研究进展[J].心血管病学进展,2023,(11):986.[doi:10.16806/j.cnki.issn.1004-3934.2023.11.007]
 HAN Bing,LAI Chunlin.Absent In Melanoma 2 Inflammasome in Cardiovascular Disease[J].Advances in Cardiovascular Diseases,2023,(11):986.[doi:10.16806/j.cnki.issn.1004-3934.2023.11.007]
点击复制

黑色素瘤缺乏因子2炎症小体在心血管疾病中的研究进展()
分享到:

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

卷:
期数:
2023年11期
页码:
986
栏目:
综述
出版日期:
2023-11-25

文章信息/Info

Title:
Absent In Melanoma 2 Inflammasome in Cardiovascular Disease
作者:
韩冰 来春林
(山西医科大学第五临床医学院心血管内科,山西 太原 030012)
Author(s):
HAN BingLAI Chunlin
(Department of Cardiovascular Medicine,The Fifth Clinical Medical College of Shanxi Medical University,Taiyuan 030012,Shanxi,China)
关键词:
黑色素瘤缺乏因子2炎症小体冠状动脉粥样硬化心肌梗死心力衰竭靶向治疗
Keywords:
inflammasomeCoronary atherosclerosisMyocardial infarctionHeart failureTargeted therapy
DOI:
10.16806/j.cnki.issn.1004-3934.2023.11.007
摘要:
黑色素瘤缺乏因子2(AIM2)可识别来自病原微生物或宿主本身的双链DNA,使活化的胱天蛋白酶-1剪切前白细胞介素-1β和前白细胞介素-18,通过介导炎症因子白细胞介素-1β和白细胞介素-18的成熟和分泌来引起固有免疫应答。此外,AIM2炎症小体可将Gasdermin D(GSDMD)转化为GSDMD-N,促进细胞因子和各种细胞质内容物的释放,导致细胞膜破裂,引起细胞焦亡。越来越多研究表明,AIM2炎症小体、白细胞介素-1β和细胞焦亡等参与了动脉粥样硬化、心肌梗死和心力衰竭等心血管疾病的发展过程。现根据目前现有研究,对AIM2炎症小体在心血管疾病发生过程中可能的作用机制做一综述,以期为心血管疾病的靶向治疗提供新思路。
Abstract:
(AIM2) recognizes double-stranded DNA from pathogenic microorganisms or the host itself,causing activated caspase-1 to shear pro-interleukin(IL)-1β and pro-IL-18 and mediating the maturation and secretion of the inflammatory factors IL-1β and IL-18 to elicit an intrinsic immune response. In addition,AIM2 inflammasome can convert Gasdermin D(GSDMD) to GSDMD-N,which promotes the release of cytokines and various cytoplasmic contents,causing cell membrane rupture and leading to pyroptosis. An increasing number of studies have shown that the development process of cardiovascular diseases,such as atherosclerosis,myocardial infarction and heart failure,is associated with AIM2 inflammasome,IL-1β and pyroptosis. This paper reviews the possible mechanisms of the role of AIM2 inflammasome in the development of cardiovascular diseases based on the current available studies,with the aim of providing new ideas for the targeted therapy of cardiovascular diseases

参考文献/References:

[1].B?k M,Yurdagul A Jr,Tabas I,et al. Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities[J]. Nat Rev Cardiol,2019,16(7):389-406.
[2].Kumari P,Russo AJ,Shivcharan S,et al. AIM2 in health and disease:inflammasomeand beyond[J]. Immunol Rev,2020,297(1):83-95.
[3].Wang L,Sun L,Byrd KM,et al. AIM2 inflammasome’s first decade of discovery:focus on oral diseases[J]. Front Immunol,2020,11:1487.
[4].Lugrin J,Martinon F. The AIM2 inflammasome:sensor of pathogens and cellular perturbations[J]. Immunol Rev,2018,281(1):99-114.
[5].Man SM,Kanneganti TD. Regulation of inflammasome activation[J]. Immunol Rev,2015,265(1):6-21.
[6].Martini E,Stirparo GG,Kallikourdis M. Immunotherapy for cardiovascular disease[J]. J Leukoc Biol,2018,103(3):493-500.
[7].Zhaolin Z,Guohua L,Shiyuan W,et al. Role of pyroptosis in cardiovascular disease[J]. Cell Prolif,2019,52(2):e12563.
[8].Geovanini GR,Libby P. Atherosclerosis and inflammation:overview and updates[J]. Clin Sci (Lond),2018,132(12):1243-1252.
[9].Li Y,Zhong X,Cheng G,et al. Hs-CRP and all-cause,cardiovascular,and cancer mortality risk:a meta-analysis[J]. Atherosclerosis,2017,259:75-82.
[10].Gimbrone MA Jr,García-Carde?a G. Endothelial cell dysfunction and the pathobiology of atherosclerosis[J]. Circ Res,2016,118(4):620-636.
[11].Yu M,Tsai SF,Kuo YM. The therapeutic potential of anti-inflammatory exerkines in the treatment of atherosclerosis[J]. Int J Mol Sci,2017,18(6):1260.
[12].Lüsebrink E,Goody PR,Lahrmann C,et al. AIM2 stimulation impairs reendothelialization and promotes the development of atherosclerosis in mice[J]. Front CardiovascMed,2020,7:582482.
[13].Pan J,Han L,Guo J,et al. AIM2 accelerates the atherosclerotic plaque progressions in ApoE-/- mice[J]. Biochem Biophys Res Commun,2018,498(3):487-494.
[14].Jaiswal S,Natarajan P,Silver AJ,et al. Clonal hematopoiesis and risk of atherosclerotic cardiovascular disease[J]. N Engl J Med,2017,377(2):111-121.
[15].Fidler TP,Xue C,Yalcinkaya M,et al. The AIM2 inflammasome exacerbates atherosclerosis in clonal haematopoiesis[J]. Nature,2021,592(7853):296-301.
[16].Opoku E,Traughber CA,Zhang D,et al. Gasdermin D mediates inflammation-induced defects in reverse cholesterol transport and promotes atherosclerosis[J]. Front Cell Dev Biol,2021,9:715211.
[17].Hakimi M,Peters A,Becker A,et al. Inflammation-related induction of absent in melanoma 2 (AIM2) in vascular cells and atherosclerotic lesions suggests a role in vascular pathogenesis[J]. J Vasc Surg,2014,59(3):794-803.
[18].Pan J,Lu L,Wang X,et al. AIM2 regulates vascular smooth muscle cell migration in atherosclerosis[J]. Biochem Biophys Res Commun,2018,497(1):401-409.
[19].Paulin N,Viola JR,Maas SL,et al. Double-strand DNA sensing AIM2 inflammasome regulates atherosclerotic plaque vulnerability[J]. Circulation,2018,138(3):321-323.
[20].Taborda NA,Blanquiceth Y,Urcuqui-Inchima S,et al. High-density lipoproteins decrease proinflammatory activity and modulate the innate immune response[J]. J Interferon Cytokine Res,2019,39(12):760-770.
[21].Gong Z,Zhang X,Su K,et al. Deficiency in AIM2 induces inflammation and adipogenesis in white adipose tissue leading to obesity and insulin resistance[J]. Diabetologia,2019,62(12):2325-2339.
[22].黄岚,王江. 心力衰竭发病机制的研究现状[J]. 中华临床医师杂志:电子版,2013,7(11):3.
[23].Krempf M,Parhofer KG,Steg PG,et al. Cardiovascular event rates in diabetic and nondiabetic individuals with and without established atherothrombosis (from the REduction of Atherothrombosis for Continued Health [REACH] registry)[J]. Am J Cardiol, 2010,105(5):667-671.
[24].Durga Devi T,Babu M,M?kinen P,et al. Aggravated postinfarct heart failure in type 2 diabetes is associated with impaired mitophagy and exaggerated inflammasome activation[J]. Am J Pathol,2017,187(12):2659-2673.
[25].Wang X,Pan J,Liu H,et al. AIM2 gene silencing attenuates diabetic cardiomyopathy in type 2 diabetic rat model[J]. Life Sci,2019,221:249-258.
[26].Onódi Z,Ruppert M,Kucsera D,et al. AIM2-driven inflammasome activation in heart failure[J]. Cardiovasc Res,2021,117(13):2639-2651.
[27].Toldo S,Kannan H,Bussani R,et al. Formation of the inflammasome in acute myocarditis[J]. Int J Cardiol,2014,171(3):e119-e121.
[28].Li Y,Bourlet T,Andreoletti L,et al. Enteroviral capsid protein VP1 is present in myocardial tissues from some patients with myocarditis or dilated cardiomyopathy[J]. Circulation,2000,101(3):231-234.
[29].Chai D,Yue Y,Xu W,et al. AIM2 co-immunization favors specific multifunctional CD8(+) T cell induction and ameliorates coxsackievirus B3-induced chronic myocarditis[J]. Antiviral Res,2015,119:68-77.
[30].Ridker PM. Residual inflammatory risk:addressing the obverse side of the atherosclerosis prevention coin[J]. Eur Heart J,2016,37(22):1720-1722.
[31].Tardif JC,Kouz S,Waters DD,et al. Efficacy and safety of low-dose colchicine after myocardial infarction[J]. N Engl J Med,2019,381(26):2497-2505.
[32].Lee KM,Kang JH,Yun M,et al. Quercetin inhibits the poly(dA:dT)-induced secretion of IL-18 via down-regulation of the expressions of AIM2 and pro-caspase-1 by inhibiting the JAK2/STAT1 pathway in IFN-γ-primed human keratinocytes[J]. Biochem Biophys Res Commun,2018,503(1):116-122.
[33].Su Q,Liu Y,Lv XW,et al. LncRNA TUG1 mediates ischemic myocardial injury bytargeting miR-132-3p/HDAC3 axis[J]. Am J Physiol Heart Circ Physiol,2020,318(2):H332-H344.
[34].Liu T,Tang Q,Liu K,et al. TRIM11 suppresses AIM2 inflammasome by degrading AIM2 via p62-dependent selective autophagy[J]. Cell Rep,2016,16(7):1988-2002.
[35].Zhang MJ,Zhao QC,Xia MX,et al. The HDAC3 inhibitor RGFP966 ameliorated ischemic brain damage by downregulating the AIM2 inflammasome[J]. FASEB J,2020,34(1):648-662.
[36].Habib P,Harms J,Zendedel A,et al. Gonadal hormones E2 and P mitigatecerebral ischemia-induced upregulation of the AIM2 and NLRC4 inflammasomes in rats[J]. Int J Mol Sci,2020,21(13):4795.

相似文献/References:

[1]程晓艺,寇秀玲,黄明刚,等.颈动脉斑块与冠状动脉粥样硬化相关性影像学分析[J].心血管病学进展,2019,(6):960.[doi:10.16806/j.cnki.issn.1004-3934.2019.06.030]
 CHENG Xiaoyi,KOU Xiuling,HUANG Minggang,et al.Imaging Analysis of Carotid Plaque and Coronary Artery Atherosclerosis[J].Advances in Cardiovascular Diseases,2019,(11):960.[doi:10.16806/j.cnki.issn.1004-3934.2019.06.030]
[2]韩月 朱莉 宋桂仙.白介素-12家族在冠状动脉粥样硬化中的研究进展[J].心血管病学进展,2020,(5):508.[doi:10.16806/j.cnki.issn.1004-3934.20.05.016]
 HAN Yue,ZHU Li,SONG Guixian.Interleukin-12 Family in Coronary Atherosclerosis[J].Advances in Cardiovascular Diseases,2020,(11):508.[doi:10.16806/j.cnki.issn.1004-3934.20.05.016]
[3]梁春晓 李爽 刘莹 余建群.不同区域的心包脂肪容积与心血管危险因素及冠状动脉粥样硬化的关系[J].心血管病学进展,2020,(8):873.[doi:10.16806/j.cnki.issn.1004-3934.2020.08.022]
 LIANG Chunxiao,LI Shuang,LIU Ying,et al.Epicardial, Paracardial and Pericardial Fat Volume by CCTA: Relationship with Cardiovascular Risk Factors and Coronary Atherosclerosis[J].Advances in Cardiovascular Diseases,2020,(11):873.[doi:10.16806/j.cnki.issn.1004-3934.2020.08.022]
[4]李爽 梁春晓 方鑫 刘莹 余建群.心包内脂肪容积对糖尿病及非糖尿病患者冠状动脉粥样硬化影响的CT评价[J].心血管病学进展,2020,(9):972.[doi:10.16806/j.cnki.issn.1004-3934.2020.09.021]
 LI Shuang,LIANG Chunxiao,FANG Xin,et al.Effect of Epicardial Adipose Tissue Volume by CCTA on Coronary Atherosclerosis in Patients with or without Type 2 Diabetes Mellitus[J].Advances in Cardiovascular Diseases,2020,(11):972.[doi:10.16806/j.cnki.issn.1004-3934.2020.09.021]
[5]王 西,王 萍.大动脉炎加速冠状动脉粥样硬化机制的研究进展[J].心血管病学进展,2022,(2):154.[doi:10.16806/j.cnki.issn.1004-3934.2022.02.015]
 WANG XiWANG Ping.Mechanism of Accelerated Atherosclerosis in Takayasu Arteritis[J].Advances in Cardiovascular Diseases,2022,(11):154.[doi:10.16806/j.cnki.issn.1004-3934.2022.02.015]
[6]谭思华 周晓莉.非酒精性脂肪肝与冠状动脉粥样硬化及炎症的研究进展[J].心血管病学进展,2023,(5):439.[doi:10.16806/j.cnki.issn.1004-3934.2023.05.013]
 TAN Sihua,ZHOU Xiaoli.Association of Non-Alcoholic Fatty Liver Disease with Coronary Atherosclerosis and Inflammation[J].Advances in Cardiovascular Diseases,2023,(11):439.[doi:10.16806/j.cnki.issn.1004-3934.2023.05.013]

更新日期/Last Update: 2023-12-13