索引超出了数组界限。 文章摘要
|本期目录/Table of Contents|

[1]戚慧茹,林瑶,石琳.川崎病合并冠状动脉瘤血管结构相关基因的研究进展[J].国际心血管病杂志,2024,02:105-108.
点击复制

川崎病合并冠状动脉瘤血管结构相关基因的研究进展(PDF)

《国际心血管病杂志》[ISSN:1006-6977/CN:61-1281/TN]

期数:
2024年02期
页码:
105-108
栏目:
综述
出版日期:
2024-03-25

文章信息/Info

Title:
-
作者:
戚慧茹; 林瑶; 石琳
100020 北京大学首都儿科研究所教学医院（戚慧茹）；100020 北京，首都儿科研究所附属儿童医院心血管内科（林瑶，石琳）
Author(s):
-
关键词:
川崎病; 冠状动脉瘤; 血管结构; 基因
Keywords:
-
分类号:
-
DOI:
10.3969/j.issn.1673-6583.2024.02.011
文献标识码:
-
摘要:
川崎病（KD）是好发于儿童的急性血管炎症性疾病，冠状动脉瘤（CAA）是KD的严重并发症，标志着更严重的临床症状和不良的临床预后。血管内膜层单核细胞浸润、内皮细胞降解以及弹性层破坏是KD合并CAA的基本病变，提示冠状动脉管壁结构存在炎症破坏。不同遗传背景的KD患儿发生CAA的风险各异，提示遗传因素在CAA发病中发挥重要作用。该文介绍KD合并CAA的血管结构相关基因和发病机制，为KD合并CAA的早期识别和机制探索提供理论依据。
Abstract:
-

参考文献/References

[1] Nakamura Y. Kawasaki disease: epidemiology and the lessons from it[J]. Int J Rheum Dis, 2018, 21(1):16-19.
[2] Sheikh AS, Hailan A, Kinnaird T, et al. Coronary artery aneurysm: evaluation, prognosis, and proposed treatment strategies[J]. Heart Views, 2019, 20(3):101-108.
[3] Singhal M, Pilania RK, Gupta P, et al. Emerging role of computed tomography coronary angiography in evaluation of children with Kawasaki disease[J]. World J Clin Pediatr, 2023, 12(3):97-106.
[4] Conte C, Sogni F, Rigante D, et al. An update on reports of atypical presentations of Kawasaki disease and the recognition of IVIG non-responder children[J]. Diagnostics Basel Switzerland, 2023, 13(8):1441.
[5] Liu WT, Liu CW, Zhang L, et al. Molecular basis of coronary artery dilation and aneurysms in patients with Kawasaki disease based on differential protein expression[J]. Mol Med Rep, 2018, 17(2):2402-2414.
[6] Matta AG, Yaacoub N, Nader V, et al. Coronary artery aneurysm:a review[J]. World J Cardiol, 2021, 13(9):446-455.
[7] Hu L, A-Zhe SGM, Zhou ZQ, et al. Quantitative assessment of myocardial edema by MR T2 mapping in children with Kawasaki disease[J]. J Magn Reson Imaging, 2023:37338016.
[8] Hayashi H, Al Mamun A, Sakima M, et al. Activator of G-protein signaling 8 is involved in VEGF-mediated signal processing during angiogenesis[J]. J Cell Sci, 2016, 129(6):1210-1222.
[9] Kim JJ, Hong YM, Yun SW, et al. Identification of rare coding variants associated with Kawasaki disease by whole exome sequencing[J]. Genomics Inform, 2021, 19(4):e38.
[10] Lin K, Zhang LY, Wang YS, et al. FNDC1 polymorphism (rs3003174 C＞T) increased the incidence of coronary artery aneurysm in patients with Kawasaki disease in a southern Chinese population[J]. J Inflamm Res, 2021, 14:2633-2640.
[11] Sato M, Jiao Q, Honda T, et al. Activator of G protein signaling 8(AGS8) is required for hypoxia-induced apoptosis of cardiomyocytes: role of G betagamma and connexin 43(CX43)[J]. J Biol Chem, 2009, 284(45):31431-31440.
[12] Runne C, Chen SH. PLEKHG2 promotes heterotrimeric G protein βγ-stimulated lymphocyte migration via Rac and Cdc42 activation and actin polymerization[J]. Mol Cell Biol, 2013, 33(21):4294-4307.
[13] Zitka O, Kukacka J, Krizkova S, et al. Matrix metalloproteinases[J]. Curr Med Chem, 2010, 17(31):3751-3768.
[14] 张园海, 李丰, 徐强, 等. 基质金属蛋白酶-9基因-1562 C/T多态性与川崎病冠脉损害及丙种球蛋白耐药的关系[J]. 医学研究杂志, 2013, 42(4):136-139.
[15] Fury W, Tremoulet AH, Watson VE, et al. Transcript abundance patterns in Kawasaki disease patients with intravenous immunoglobulin resistance[J]. Hum Immunol, 2010, 71(9):865-873.
[16] Shimizu C, Matsubara T, Onouchi Y, et al. Matrix metalloproteinase haplotypes associated with coronary artery aneurysm formation in patients with Kawasaki disease[J]. J Hum Genet, 2010, 55(12):779-784.
[17] Ikeda K, Ihara K, Yamaguchi K, et al. Genetic analysis of MMP gene polymorphisms in patients with Kawasaki disease[J]. Pediatr Res, 2008, 63(2):182-185.
[18] Mirhafez SR, Avan A, Tajfard M, et al. Relationship between serum cytokines receptors and matrix metalloproteinase 9 levels and coronary artery disease[J]. J Clin Lab Anal, 2017, 31(5):e22100.
[19] Yang YN, Hu XB. The predictive values of MMP-9, PLTs, ESR, and CRP levels in Kawasaki disease with cardiovascular injury[J]. Evid Based Complement Alternat Med, 2022, 2022:6913315.
[20] 丛晓辉, 塔依尔·斯拉吉, 祖丽皮娅·黑力木, 等. 基质金属蛋白酶-9、抗内皮细胞抗体和抗中性粒细胞胞浆抗体在川崎病冠状动脉损害中的作用及临床意义[J]. 中国妇幼保健, 2019, 34(10):2284-2286.
[21] Senzaki H, Masutani S, Kobayashi J, et al. Circulating matrix metalloproteinases and their inhibitors in patients with Kawasaki disease[J]. Circulation, 2001, 104(8):860-863.
[22] Kauskot A, Vandenbriele C, Louwette S, et al. PEAR1 attenuates megakaryopoiesis via control of the PI3K/PTEN pathway[J]. Blood, 2013, 121(26):5208-5217.
[23] Pi L, Xu YF, Fu LY, et al. A PEAR1 polymorphism (rs12041331)is associated with risk of coronary artery aneurysm in Kawasaki disease[J]. Ann Hum Genet, 2019, 83(1):54-62.
[24] Vandenbriele C, Kauskot A, Vandersmissen I, et al. Platelet endothelial aggregation receptor-1: a novel modifier of neoangiogenesis[J]. Cardiovasc Res, 2015, 108(1):124-138.
[25] Fisch AS, Yerges-Armstrong LM, Backman JD, et al. Genetic variation in the platelet endothelial aggregation receptor 1 gene results in endothelial dysfunction[J]. PLoS One, 2015, 10(9):e0138795.
[26] Norton GR, Brooksbank R, Woodiwiss AJ. Gene variants of the renin-angiotensin system and hypertension: from a trough of disillusionment to a welcome phase of enlightenment?[J]. Clin Sci (Lond), 2010, 118(8):487-506.
[27] Takeuchi K, Yamamoto K, Kataoka S, et al. High incidence of angiotensin I converting enzyme genotype Ⅱ in Kawasaki disease patients with coronary aneurysm[J]. Eur J Pediatr, 1997, 156(4):266-268.
[28] Liu YF, Fu LY, Pi L, et al. An angiotensinogen gene polymorphism (rs5050) is associated with the risk of coronary artery aneurysm in southern Chinese children with Kawasaki disease[J]. Dis Markers, 2019, 2019:2849695.
[29] Simonyte S, Kuciene R, Medzioniene J, et al. Renin-angiotensin system gene polymorphisms and high blood pressure in Lithuanian children and adolescents[J]. BMC Med Genet, 2017, 18(1):100.
[30] Shimizu C, Jain S, Davila S, et al. Transforming growth factor-beta signaling pathway in patients with Kawasaki disease[J]. Circ Cardiovasc Genet, 2011, 4(1):16-25.
[31] Choi YM, Shim KS, Yoon KL, et al. Transforming growth factor beta receptor Ⅱ polymorphisms are associated with Kawasaki disease[J]. Korean J Pediatr, 2012, 55(1):18-23.
[32] 史翠平, 张宏艳. TGFBR2基因多态性与川崎病和冠状动脉损伤相关性的研究[J]. 中国当代儿科杂志, 2013, 15(9):767-770.
[33] Chen YT, Liao WL, Lin YJ, et al. Association between SRC-1 gene polymorphisms and coronary artery aneurysms formation in Taiwanese children with Kawasaki disease[J]. J Clin Lab Anal, 2014, 28(6):435-439.
[34] Inamoto S, Kwartler CS, Lafont AL, et al. TGFBR2 mutations alter smooth muscle cell phenotype and predispose to thoracic aortic aneurysms and dissections[J]. Cardiovasc Res, 2010, 88(3):520-529.
[35] Tsamis A, Krawiec JT, Vorp DA. Elastin and collagen fibre microstructure of the human aorta in ageing and disease: a review[J]. J R Soc Interface, 2013, 10(83):20121004.
[36] Nabower AM, Starr LJ, Cramer J. Kawasaki disease in a patient with williams syndrome[J]. World J Pediatr Congenit Heart Surg, 2020, 11(4):NP144-NP147.
[37] Lau AC, Duong TT, Ito S, et al. Matrix metalloproteinase 9 activity leads to elastin breakdown in an animal model of Kawasaki disease[J]. Arthritis Rheum, 2008, 58(3):854-863.
[38] Rajasekaran K, Duraiyarasan S, Adefuye MYA, et al. Kawasaki disease and coronary artery involvement: a narrative review[J]. Cureus, 2022, 14(8):e28358.

备注/Memo

备注/Memo:
基金项目：北京亦城合作发展基金会（YCXJ-JZ-2022-007）
通信作者：石琳，E-mail：shilin9789@126.com
更新日期/Last Update: 2024-03-25