痛风的多组学研究进展

doi:10.16288/j.yczz.23-086

遗传 ›› 2023, Vol. 45 ›› Issue (8): 643-657.doi: 10.16288/j.yczz.23-086

痛风的多组学研究进展

时文睿^1,^2,³(), 渠鸿竹^1,^2,³(), 方向东^1,^2,³()

1.中国科学院北京基因组研究所（国家生物信息中心），中国科学院基因组科学与信息重点实验室，北京 100101
2.中国科学院大学，北京 100049
3.基因组与精准医学检测技术北京市重点实验室，北京 100101

收稿日期:2023-04-03 修回日期:2023-06-13 出版日期:2023-08-20 发布日期:2023-06-28
通讯作者: 渠鸿竹,方向东 E-mail:shiwenrui@big.ac.cn;quhongzhu@big.ac.cn;fangxd@big.ac.cn
作者简介:时文睿，在读硕士研究生，专业方向：基因组学。E-mail: shiwenrui@big.ac.cn
基金资助:
国家重点研发计划项目(2022YFC2503304);国家自然科学基金(82220108015)

Overview of multi-omics research in gout

Wenrui Shi^1,^2,³(), Hongzhu Qu^1,^2,³(), Xiangdong Fang^1,^2,³()

1. CAS Key Laboratory of Genome Sciences and Information, Beijing Institute of Genomics, Chinese Academy of Sciences/China National Center for Bioinformation, Beijing 100101, China
2. University of Chinese Academy of Sciences, Beijing 100049, China
3. Beijing Key Laboratory of Genome and Precision Medicine Technologies, Beijing 100101, China

Received:2023-04-03 Revised:2023-06-13 Online:2023-08-20 Published:2023-06-28
Contact: Hongzhu Qu,Xiangdong Fang E-mail:shiwenrui@big.ac.cn;quhongzhu@big.ac.cn;fangxd@big.ac.cn
Supported by:
National Key Research and Development Program of China(2022YFC2503304);National Natural Science Foundation of China(82220108015)

摘要/Abstract

摘要：

痛风是一种由尿酸盐结晶沉积引起的自限性炎症疾病，伴有多种合并症。随着生活水平的提高，痛风在全球的发病率逐年上升，严重影响人民健康。组学技术是研究疾病的有效工具，已被广泛应用于发现痛风的潜在生物标志物和风险因子，其鉴定出的变异位点或差异表达产物为研究痛风的发病机制和疾病进展提供了不同维度的见解和认识。本文通过PubMed检索相关文献，分析和总结了多组学技术在痛风中的应用和研究结果，对近年来多组学技术在痛风领域的相关研究进展进行综述，以期了解痛风患者在不同分子层次上的特异性变化，为今后更深入地研究痛风提供思路和方向。

关键词: 痛风, 基因组学, 表观基因组学, 转录组学, 蛋白组学

Abstract:

Gout is a self-limiting inflammation disease triggered by deposition of monosodium urate with a variety of comorbidities. With the improvement of living standards, the global incidence of gout is increasing year by year, which seriously affects people's health. As an effective tool to study diseases, omics technology has been widely used to discover potential biomarkers and risk factors of gout. The identified variation sites or different-expressed products provide different dimensions of insights for the study of the pathogenesis and disease progression of gout. In this review, the application and research results of multi-omics technology in gout were analyzed and summarized through PubMed literature retrieval. Meanwhile, the recent research progress of multi-omics technology in the field of gout was reviewed to understand the specific changes of gout patients at different molecular levels, and to provide ideas and directions for further research on gout in the future.

Key words: gout, genomics, epigenomics, transcriptomics, proteomics

时文睿, 渠鸿竹, 方向东. 痛风的多组学研究进展[J]. 遗传, 2023, 45(8): 643-657.

Wenrui Shi, Hongzhu Qu, Xiangdong Fang. Overview of multi-omics research in gout[J]. Hereditas(Beijing), 2023, 45(8): 643-657.

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研究方法	队列来源	样本量	痛风风险基因	参考文献
GWAS分析	英国	7049例痛风，81,354例AH对照	ABCG2、SLC2A9、SLC22A11、GCKR、MEPE、PPM1K-DT、LOC105377323、ADH1B	[23]
	德国	1217例痛风，3724例肾病患者	SLC2A9、ABCG2	[24]
	欧洲，美国	63,031例受试者	PKD2、SLC2A9、SLC17A1、SLC17A4、SLC17A2	[25]
	日本	2860例痛风，3149例AH对照	CNTN5，MIR302F、ZNF724	[26]
	日本	1411例痛风，1285例健康对照	A1CF、BAZ1B	[27]
	中国台湾	758例痛风，14,166例健康对照	PKD2、NUTD9、NAP1L5	[28]
	中国台湾，日本	3800例痛风，6625例健康对照	FGF5、MLXIP	[29]
	中国台湾	952例痛风，11,650例AH对照，46,870例健康对照	SLC2A9、C5orf22、SPANXN1、CNTNAP2、GLRX5	[34]
	中国台湾	5857例痛风患者，12,382例AH对照，21,355例健康对照	DNAJC16、AGMAT、NUDT17、TRIM46、MUC1MTX1	[35]
WES分析	中国	5例痛风，4例健康对照（同一家系）	LRP1、OIT3	[36]
	中国	5例痛风，1例AH患者，7例健康对照（同一家系）	CPT2	[37]
	中国	2例痛风，3例健康对照（同一家系）	SLC16A9	[38]
	中国	2例痛风，2例健康对照（第一家系）、3例痛风，8例健康对照（第二家系）、4例痛风，5例健康对照（第三家系）	ABCG2、PRKG2、ADRB3	[39]

RNA类型	RNA分子	靶向基因/miRNA	表征	参考文献
mRNA	NLRP3-4↓	NLRP3	IL-1β升高、NLRP3炎症小体降低	[56]
mRNA	PTGS2、NFE2L2↑/ CASP8、CD274↓	miR-128-3p、miR-20a-5p、miR-16-5p、miR-155-5p	促进细胞炎症性坏死	[57]
miRNA	miR-488、miR-920↓	IL1B	炎症细胞因子水平升高	[61]
	miR-192-5p↓	EREG	炎症细胞因子水平升高、M1巨噬细胞活化	[62]
	miR-223-3p、miR-22-3p↓	NLRP3	炎症细胞因子水平升高	[63]
	miR-142-3p↑	ZEB2	激活NF-κB信号通路、炎症细胞因子水平升高	[64]
	miR-221-5p↓	IL1B	炎症细胞因子水平升高	[65]
	miR-339-5p、miR-486-5p、miR-361-5p↓	-	趋化因子配体2水平升高、炎症细胞因子水平升高	[66]
	miR-302b↑	IRAK4、EphA2	抑制NF-κB和半胱天冬酶-1信号通路、抑制巨噬细胞迁移、炎症细胞因子水平降低	[67]
	miR-146a↑	TRAF6、IRAK1	炎症细胞因子水平降低	[68]
	miR-155↑	SHIP-1	炎症细胞因子水平升高	[69]
lncRNA	lncRNA-MM2P↓	-	炎症细胞因子水平升高	[75]
lncRNA	lncRNA-H19↑	miR-22-3p	激活NF-κB信号通路、炎症细胞因子水平升高	[76]
ceRNA	lncRNA-HOTAIR↑/miR-20b↓	NLRP3	炎症细胞因子水平升高	[83]
	lncRNA-SNHG8↑/miR-542-3p↓	AP3D1	炎症细胞因子水平升高	[84]
	circHIPK3↑/miR-192、miR-561↓	TLR4、NLRP3	激活TLR4信号通路、炎症细胞因子水平升高	[85]
	lncRNA-NEAT1↑/miR-142-3p↓	IL-6	炎症细胞因子水平升高	[58]

样本类型	参与者数量	重要代谢物	涉及代谢通路	参考文献
尿液	29名健康对照，35名痛风患者	乙醇胺、苯乙醇胺、乙醇酸盐、甘油、半乳糖醛酸、硬脂酸酯、琥珀酸盐、延胡索酸酯、丙二醇、5-羟基-L-色氨酸、5-羟基吲哚-3-乙酸酯、β-乳酸、苏氨酸盐、D-来苏糖、核糖醇、山梨糖醇、D-醛糖、葡萄糖酸盐、尿嘧啶、尿酸盐、肌酐，异黄蝶呤、氨基酸类	嘌呤核苷酸合成、氨基酸代谢、嘌呤代谢、脂质代谢、碳水化合物代谢、三羧酸循环	[92]
血浆	29名健康对照，20名AH患者，20名痛风患者	L-异亮氨酸、L-赖氨酸、L-丙氨酸	-	[97]
血浆	26名健康对照，26名痛风患者	白三烯B4	-	[99]
血清	50名健康对照，50名AH患者，49名痛风患者	极低密度脂蛋白、脂质、谷氨酰胺、丙酮、柠檬酸盐、肌酸酐、β-葡萄糖、α-葡萄糖、甘油三酯、不饱和脂质、氨基酸类	氨酰基-tRNA生物合成、支链氨基酸生物合成、D-谷氨酰胺，D-谷氨酸代谢	[95]
血清	31名健康对照，31名痛风患者	4-羟基三唑仑、尿酸盐、胆红素	胆汁酸生物合成、嘌呤代谢、甘油磷脂代谢	[96]
血清，尿液	30名健康对照，30名痛风患者	次黄嘌呤、黄嘌呤、焦谷氨酸、2-甲基丁酰肉碱、氨基酸类	嘌呤代谢、支链氨基酸代谢、三羧酸循环、酮体的合成和降解、胆汁分泌、花生四烯酸代谢	[98]
血清	80名健康对照，62名AH患者，69名痛风患者	犬尿喹啉酸、5-羟基吲哚乙酸	-	[100]

痛风的多组学研究进展

Overview of multi-omics research in gout

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