切换至 "中华医学电子期刊资源库"

中华老年病研究电子杂志 ›› 2023, Vol. 10 ›› Issue (04) : 47 -49. doi: 10.3877/cma.j.issn.2095-8757.2023.04.008

综述

高尿酸血症促进冠状动脉钙化的研究进展
龚小燕1, 陈庆伟1,()   
  1. 1. 400010 重庆,重庆医科大学附属第二医院全科医学科
  • 收稿日期:2023-10-01 出版日期:2023-11-28
  • 通信作者: 陈庆伟

The association between hyperuricemia and coronary artery calcification

Xiaoyan Gong1, Qingwei Chen1,()   

  1. 1. Department of General Practice, the Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China
  • Received:2023-10-01 Published:2023-11-28
  • Corresponding author: Qingwei Chen
引用本文:

龚小燕, 陈庆伟. 高尿酸血症促进冠状动脉钙化的研究进展[J/OL]. 中华老年病研究电子杂志, 2023, 10(04): 47-49.

Xiaoyan Gong, Qingwei Chen. The association between hyperuricemia and coronary artery calcification[J/OL]. Chinese Journal of Geriatrics Research(Electronic Edition), 2023, 10(04): 47-49.

高尿酸血症是一种常见的代谢性疾病,其病理损伤并不局限于肾脏、关节等部位,可引起一系列全身性炎症反应。研究发现,高尿酸血症可能通过促进炎症反应、诱导氧化应激等促进冠状动脉钙化的发生和发展,且与高血压、糖尿病等冠心病危险因素相互影响,增加冠状动脉钙化的风险。在基因层面,孟德尔随机化研究也为高尿酸血症与冠状动脉疾病存在关联提供了新的证据。本文对高尿酸血症与冠状动脉钙化之间的关系进行综述,旨在厘清高尿酸血症影响冠状动脉钙化的可能机制,为冠状动脉钙化的防治和干预提供新的思路。

Hyperuricemia is a common metabolic disease, whose pathological damage is not limited to kidney, joint and other parts, but can cause a series of systemic inflammatory reactions. Studies have found that hyperuricemia may promote the occurrence and development of coronary artery calcification by promoting inflammatory response and inducing oxidative stress, and interact with coronary heart disease risk factors such as hypertension and diabetes to increase the risk of coronary artery calcification. At the genetic level, mendelian randomization studies have also provided new evidence for the association between hyperuricemia and coronary artery disease. This article reviews the relationship between hyperuricemia and coronary artery calcification, aiming to clarify the possible mechanism of hyperuricemia affecting coronary artery calcification, and provide new ideas for the prevention and treatment of coronary artery calcification.

[1]
Chen-Xu M, Yokose C, Rai SK, et al. Contemporary prevalence of gout and hyperuricemia in the United States and decadal trends: The National Health and Nutrition Examination Survey, 2007-2016[J]. Arthritis Rheumatol, 2019, 71(6):991-999.
[2]
Liu R, Han C, Wu D, et al. Prevalence of hyperuricemia and gout in mainland China from 2000 to 2014: A systematic review and meta-analysis[J]. Biomed Res Int, 2015, 2015:762820.
[3]
Li Y, Shen Z, Zhu B, et al. Demographic, regional and temporal trends of hyperuricemia epidemics in mainland China from 2000 to 2019: A systematic review and meta-analysis[J]. Glob Health Action, 2021, 14(1):1874652.
[4]
Jun JE, Lee YB, Lee SE, et al. Elevated serum uric acid predicts the development of moderate coronary artery calcification independent of conventional cardiovascular risk factors[J]. Atherosclerosis, 2018, 272:233-239.
[5]
Kiss LZ, Bagyura Z, Csobay-Novák C, et al. Serum uric acid is independently associated with coronary calcification in an asymptomatic population[J]. J Cardiovasc Transl Res, 2019, 12(3):204-210.
[6]
Liang L, Hou X, Bainey KR, et al. The association between hyperuricemia and coronary artery calcification development: A systematic review and meta-analysis[J]. Clin Cardiol, 2019, 42(11):1079-1086.
[7]
Wang X, Liu X, Qi Y, et al. High level of serum uric acid induced monocyte inflammation is related to coronary calcium deposition in the middle-aged and elder population of China: A five-year prospective cohort study[J]. J Inflamm Res, 2022, 15:1859-1872.
[8]
Luis-Rodríguez D, Donate-Correa J, Martín-Núñez E, et al. Serum urate is related to subclinical inflammation in asymptomatic hyperuricaemia[J]. Rheumatology (Oxford), 2021, 60(1):371-379.
[9]
Agrawal M, Niroula A, Cunin P, et al. TET2-mutant clonal hematopoiesis and risk of gout[J]. Blood, 2022,140(10):1094-1103.
[10]
Doğru S, Yaşar E, Yeşilkaya A. Uric acid can enhance MAPK pathway-mediated proliferation in rat primary vascular smooth muscle cells via controlling of mitochondria and caspase-dependent cell death[J]. J Recept Signal Transduct Res, 2022, 42(3):293-301.
[11]
Kimura Y, Yanagida T, Onda A, et al. Soluble uric acid promotes atherosclerosis via ampk (amp-activated protein kinase)-mediated inflammation[J]. Arterioscler Thromb Vasc Biol, 2020, 40(3):570-582.
[12]
Chen M, Lu X, Lu C, et al. Soluble uric acid increases PDZK1 and ABCG2 expression in human intestinal cell lines via the TLR4-NLRP3 inflammasome and PI3K/Akt signaling pathway[J]. Arthritis Res Ther, 2018,20(1):20.
[13]
Roumeliotis S, Roumeliotis A, Dounousi E, et al. Dietary antioxidant supplements and uric acid in chronic kidney disease: A review[J]. Nutrients, 2019, 11(8):1911.
[14]
Song C, Zhao X. Uric acid promotes oxidative stress and enhances vascular endothelial cell apoptosis in rats with middle cerebral artery occlusion[J]. Biosci Rep, 2018, 38(3):BSR20170939.
[15]
Borghi C, Rosei EA, Bardin T, et al. Serum uric acid and the risk of cardiovascular and renal disease[J]. J Hypertens, 2015, 33(9):1729-1741.
[16]
Yuan H, Yu C, Li X, et al. Serum uric acid levels and risk of metabolic syndrome: A dose-response meta-analysis of prospective studies[J]. J Clin Endocrinol Metab, 2015, 100(11):4198-4207.
[17]
Wang J, Qin T, Chen J, et al. Hyperuricemia and risk of incident hypertension: A systematic review and meta-analysis of observational studies[J/OL]. PLoS One, 2014, 9(12):e114259.
[18]
Lv Q, Meng XF, He FF, et al. High serum uric acid and increased risk of type 2 diabetes: A systemic review and meta-analysis of prospective cohort studies[J/OL]. PLoS One, 2013, 8(2):e56864.
[19]
Maloberti A, Biolcati M, Ruzzenenti G, et al. The role of uric acid in acute and chronic coronary syndromes[J]. J Clin Med, 2021,10(20):4750.
[20]
White J, Sofat R, Hemani G, et al. Plasma urate concentration and risk of coronary heart disease: A Mendelian randomisation analysis[J]. Lancet Diabetes Endocrinol, 2016, 4(4):327-336.
[21]
Kleber ME, Delgado G, Grammer TB, et al. Uric acid and cardiovascular events: A mendelian randomization study[J]. J Am Soc Nephrol, 2015, 26(11):2831-2838.
[22]
Borghi C, Domienik-Karłowicz J, Tykarski A, et al. Expert consensus for the diagnosis and treatment of patient with hyperuricemia and high cardiovascular risk: 2021 update[J]. Cardiol J, 2021, 28(1):1-14.
[1] 周容, 张亚萍, 廖宇, 程晓萍, 管玉龙, 潘广玉, 闫杰, 王贤芝, 苟中山, 潘登科, 李巅远. 超声在基因编辑猪-猴异种并联式心脏移植术中的应用价值[J/OL]. 中华医学超声杂志(电子版), 2024, 21(06): 617-623.
[2] 王振宇, 张洪美, 荆琳, 何名江, 闫奇. 膝骨关节炎相关炎症因子与血浆代谢物间的因果关系及中介效应[J/OL]. 中华损伤与修复杂志(电子版), 2024, 19(06): 467-473.
[3] 奚卫, 王闻卿, 刘玥, 王亚楠, 许学斌. 胃肠炎继发脓毒症感染创伤弧菌ST14514的病原学诊断与文献病例回顾分析[J/OL]. 中华实验和临床感染病杂志(电子版), 2024, 18(05): 293-302.
[4] 张洁, 罗小霞, 余鸿. 系统性免疫炎症指数对急性胰腺炎患者并发器官功能损伤的预测价值[J/OL]. 中华普外科手术学杂志(电子版), 2025, 19(01): 68-71.
[5] 唐梅, 周丽, 牛岑月, 周小童, 王倩. ICG荧光导航的腹腔镜肝切除术临床意义[J/OL]. 中华普外科手术学杂志(电子版), 2024, 18(06): 655-658.
[6] 付成旺, 杨大刚, 王榕, 李福堂. 营养与炎症指标在可切除胰腺癌中的研究进展[J/OL]. 中华普外科手术学杂志(电子版), 2024, 18(06): 704-708.
[7] 高娟, 徐建庆, 闫芳, 丁盛华, 刘霞. Rutkow、TAPP、TEP 手术治疗单侧腹股沟疝患者的临床疗效及对血清炎症因子水平的影响[J/OL]. 中华疝和腹壁外科杂志(电子版), 2024, 18(06): 675-680.
[8] 刘文竹, 唐窈, 刘付臣. 诱导多潜能干细胞在神经肌肉疾病研究中的应用进展[J/OL]. 中华细胞与干细胞杂志(电子版), 2024, 14(06): 367-373.
[9] 孙璐, 蒋亚玲, 陈凌君. 布托啡诺对脑缺血再灌注损伤大鼠神经炎症和JAK2/STAT3信号通路的影响[J/OL]. 中华细胞与干细胞杂志(电子版), 2024, 14(06): 344-350.
[10] 周敏, 徐阳, 胡莹, 黄先凤. 维持性血液透析患者血清β-CTX、N-MID 和PICP 与冠状动脉钙化的关系及其诊断价值[J/OL]. 中华肾病研究电子杂志, 2024, 13(05): 256-260.
[11] 杜霞, 马梦青, 曹长春. 造影剂诱导的急性肾损伤的发病机制及干预靶点研究进展[J/OL]. 中华肾病研究电子杂志, 2024, 13(05): 279-282.
[12] 陈倩倩, 袁晨, 刘基, 尹婷婷. 多层螺旋CT 参数、癌胚抗原、错配修复基因及病理指标对结直肠癌预后的影响[J/OL]. 中华消化病与影像杂志(电子版), 2024, 14(06): 507-511.
[13] 丁富贵, 吴泽涛, 董卫国. 家族性腺瘤性息肉病临床特征及生物信息学分析[J/OL]. 中华消化病与影像杂志(电子版), 2024, 14(06): 512-518.
[14] 王湛, 李文坤, 杨奕, 徐芳, 周敏思, 苏珈仪, 王亚丹, 吴静. 炎症指标在早发性结直肠肿瘤中的应用[J/OL]. 中华临床医师杂志(电子版), 2024, 18(09): 802-810.
[15] 李玺, 蔡芸莹, 张永红, 苏恒. 假性软骨发育不全合并1型糖尿病一例[J/OL]. 中华临床医师杂志(电子版), 2024, 18(05): 518-520.
阅读次数
全文


摘要