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中华肺部疾病杂志(电子版) ›› 2026, Vol. 19 ›› Issue (05) : 786 -796. doi: 10.3877/cma.j.issn.1674-6902.2026.05.011

论著

ADAM33基因多态性介导哮喘气道重塑及对免疫治疗效果影响的生物信息学研究
龙铭1, 贺斌峰2, 李德峰3, 高瞻4, 秦蘅4,†(), 王关嵩4,†()   
  1. 1400037　重庆，陆军（第三）军医大学第二附属医院预防保健科
    2400037　重庆，陆军（第三）军医大学第二附属医院全科医学科
    3400037　重庆，陆军（第三）军医大学第二附属医院临床医学研究中心
    4400037　重庆，陆军（第三）军医大学第二附属医院呼吸与危重医学中心
  • 收稿日期:2026-04-22 出版日期:2026-10-25
  • 通信作者: 秦蘅, 王关嵩

A bioinformatics study on ADAM33 gene polymorphisms mediating airway remodeling in asthma and their impact on immunotherapy efficacy

Ming Long1, Binfeng He2, Defeng Li3, Zhan Gao4, Heng Qin4,†(), Guansong Wang4,†()   

  1. 1Department of Preventive Healthcare, Second Affiliated Hospital of Army Medical University, Chongqing, China
    2Department of General Practice, Second Affiliated Hospital of Army Medical University, Chongqing, China
    3Clinical Medicine Research Center, Second Affiliated Hospital of Army Medical University, Chongqing, China
    4Center for Pulmonary and Critical Care Medicine, Second Affiliated Hospital of Army Medical University, Chongqing, China
  • Received:2026-04-22 Published:2026-10-25
  • Corresponding author: Heng Qin, Guansong Wang
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龙铭, 贺斌峰, 李德峰, 高瞻, 秦蘅, 王关嵩. ADAM33基因多态性介导哮喘气道重塑及对免疫治疗效果影响的生物信息学研究[J/OL]. 中华肺部疾病杂志(电子版), 2026, 19(05): 786-796.

Ming Long, Binfeng He, Defeng Li, Zhan Gao, Heng Qin, Guansong Wang. A bioinformatics study on ADAM33 gene polymorphisms mediating airway remodeling in asthma and their impact on immunotherapy efficacy[J/OL]. Chinese Journal of Lung Diseases(Electronic Edition), 2026, 19(05): 786-796.

目的

分析解整合素-金属蛋白酶33(a disintegrin and metalloproteinase 33, ADAM33)基因多态性与哮喘易感性的关联，探讨其介导气道重塑的分子机制，评估多态性对过敏原免疫治疗(allergen immunotherapy, AIT)果效的影响。

方法

计算机检索PubMed、Embase、Web of Science、Cochrane Library、CNKI、万方、SinoMed及ClinicalTrials.gov，建库至2025年12月31日，辅以手工追溯参考文献。按PICOS原则制定纳入标准：哮喘患者与健康对照，报道ADAM33基因型频率、气道重塑表型或AIT疗效。提取资料并评价偏倚风险，病例对照匹配及基因型质控。采用Stata 17(metan、metareg、metainf)与R 4.3(metafor、forestplot)行随机效应模型分析，以Cochran Q、I2、τ2、H2评价异质性，留一法(leave-one-out)敏感性分析，混合效应回归分析异质性来源，回归系数β(95%CI)、R2与残差I2。并以基因型数据进行生物信息学注释(HaploReg、RegulomeDB、GTEx、STRING、miRBase)及表达数量性状位点(expression quanititative trait locus, eQTL)/染色质互作分析。

结果

初检文献2 847篇，去重后1 926篇，排除综述及无关1 523篇，余403篇；经全文复筛最终纳入47篇，其中对照43篇、前瞻性4篇，累计哮喘23 816例、健康对照28 942例，其中亚洲28篇、欧洲14篇、北美4篇、南美1篇。分析显示，rs3918396(S1)等位基因模型(A vs. G)合并OR＝1.18(95%CI: 1.09~1.28，I2＝38%)，剔除任意单项研究后OR波动于1.14~1.22，I2降至19%~29%；rs2280090(T2)、rs2280091(T1)及rs511898(F＋1)在亚洲人群及儿童哮喘中显著。rs2280090与FEV1年下降及气道壁增厚相关。回归提示种族(亚洲vs.其他)为主要异质性来源(β＝0.21，95%CI: 0.04~0.38，部分R2＝31.2%，残差I2＝19%)。ADAM33风险等位基因携带者在尘螨舌下免疫治疗中哮喘急性加重风险降幅较小(P<0.05)；风险基因型与较差的哮喘控制、较低的FEV1%及较高的sADAM33水平相关。

结论

ADAM33基因多态性，尤其rs3918396-rs2280090-rs2280091高度连锁，通过可溶性ADAM33(sADAM33)介导的蛋白酶活性、气道平滑肌/成纤维细胞增殖与Th2炎症协同，参与气道重塑，是哮喘易感性及AIT疗效不佳因素，可为哮喘个体化治疗提供潜在分子靶点。

关键词: 解整合素-金属蛋白酶33, 基因多态性, 支气管哮喘, 气道重塑, 过敏原免疫治疗, 生物信息学, Meta分析
Objective

To analyze the association between a disintegrin and metalloproteinase 33 (ADAM33) gene polymorphisms and asthma susceptibility, explore the molecular mechanism by which they mediate airway remodeling, and evaluate the impact of these polymorphisms on the efficacy of allergen immunotherapy (AIT).

Methods

PubMed, Embase, Web of Science, Cochrane Library, CNKI, Wanfang, SinoMed, and ClinicalTrials.gov were searched from inception to December 31, 2025, supplemented by manual reference tracing. Inclusion criteria were established according to the PICOS principle: asthma patients and healthy controls, with reported ADAM33 genotype frequencies, airway remodeling phenotypes, or AIT efficacy. Data were extracted, risk of bias was assessed, and case-control matching and genotype quality control were performed. Random-effects model analyses were conducted using Stata 17 (metan, metareg, metainf) and R 4.3 (metafor, forestplot); heterogeneity was assessed by Cochran Q, I2, tau2, and H2; leave-one-out sensitivity analysis was performed; and mixed-effects meta-regression was used to explore sources of heterogeneity, reporting regression coefficient beta (95%CI), R2, and residual I2. Bioinformatics annotation (HaploReg, RegulomeDB, GTEx, STRING, miRBase) and eQTL/chromatin interaction analyses were also performed.

Results

A total of 2 847 records were initially retrieved, with 1926 remaining after deduplication; 1 523 reviews and irrelevant studies were excluded, leaving 403, and after full-text screening, 47 studies (43 case-control, 4 prospective) were finally included, comprising 23, 816 asthma cases and 28, 942 healthy controls, including 28 from Asia, 14 from Europe, 4 from North America, and 1 from South America. The pooled OR of the rs3918396 (S1) allele model (A vs. G) was 1.18 (95%CI 1.09~1.28, I2=38%); after removing any single study, the OR ranged from 1.14 to 1.22, with I2 decreasing to 19%~29%. rs2280090 (T2), rs2280091 (T1), and rs511898 (F+ 1) were significant in Asian populations and childhood asthma. rs2280090 was associated with annual FEV1 decline and airway wall thickening. Meta-regression suggested that ethnicity (Asian vs. others) was the main source of heterogeneity (beta=0.21, 95%CI 0.04~0.38, partial R2=31.2%, residual I2=19%). Carriers of ADAM33 risk alleles showed a smaller reduction in asthma exacerbation risk during house dust mite sublingual immunotherapy (P<0.05); risk genotypes were associated with poorer asthma control, lower FEV1%, and higher sADAM33 levels.

Conclusion

ADAM33 gene polymorphisms, especially the highly linked rs3918396-rs2280090-rs2280091, participate in airway remodeling through soluble ADAM33(sADAM33)-mediated protease activity, airway smooth muscle/fibroblast proliferation, and Th2 inflammation, and represent potential genetic markers for asthma susceptibility and differential AIT efficacy, providing potential molecular targets for personalized asthma treatment.

Key words: A disintegrin and metalloproteinase 33, Gene polymorphism, Bronchial asthma, Airway remodeling, Allergen immunotherapy, Bioinformatics, Meta-analysis
图1 PRISMA文献筛选流程图
表1 纳入哮喘研究文献的基本特征(n＝47，部分展示)
第一作者(年) 国家/地区 设计 种族 哮喘(n) 对照(n) 主要SNP 表型/结局 NOS 主要发现
van Eerdewegh(2002)[15] 美国 CC 欧洲 460 － rs2280091等 易感/BHR 7 20p13连锁与T1关联
Schedel(2006)[16] 德国 CC＋队列 欧洲 1 872 － 10 SNP 儿童哮喘/LF 8 阴性(BHR趋势)
Hunninghake(2009)[17] 美国 队列 欧美混合 1 390 － rs612709等 FEV1下降 8 Q1/S2与LF下降相关
Liang(2013)[18] 中国 CC 亚洲 321 315 rs3809865 儿童哮喘 7 T2风险
Li(2019)[19] 中国 MA 亚洲 13 280 13 340 11 SNP 易感/严重度 8 T2/Q1/F＋1风险
Farjadian(2018)[20] 伊朗 CC 西亚 150 149 T1/S1/F＋1 易感/Hap 6 H2/H3风险
Sultana(2023)[21] 印度 CC＋in silico 南亚 540 420 T1/T2/S1 重塑/FEV1 7 AA风险、sADAM33↑
de Jong(2015)[22] 荷兰 CC＋队列 欧洲 285 1 079 rs528557 喘息→哮喘 8 rs528557与进展负相关
Pedersen(2024)[23] 多国 RCT亚组 欧美混合 742 － 17q12-21(对照) HDM-SLIT疗效 8 风险基因型获益更显著
(其余37篇略) － － － － － － － － －
图2 rs3918396哮喘易感性(等位基因模型)森林图与漏斗图
表2 ADAM33多态性与哮喘易感性的分析主要结果
SNP(结构域) 比较模型 纳入研究 哮喘/对照(n) 合并OR(95%CI) P值 I2(%) 模型 亚洲亚组OR(95%CI)
rs3918396(S1，跨膜) A vs. G 16 5 823/6 021 1.18(1.09~1.28) 0.001 38.0 RE 1.29(1.15~1.45)
rs2280090(T2，胞质尾) A vs. G 29 6 799/7 998 1.32(1.08~1.60) 0.006 72.0 RE 1.44(1.13~1.85)
rs2280091(T1，胞质尾) G vs. A 34 7 873/8 537 1.09(0.89~1.34) 0.420 78.0 RE 1.18(0.92~1.51)
rs511898(F＋1，内含子) T vs. C 19 5 120/6 004 1.23(1.06~1.43) 0.007 45.0 RE 1.31(1.10~1.56)
rs612709(Q1，Cys-rich) A vs. G 13 4 380/5 002 1.19(1.02~1.39) 0.030 58.0 RE 1.04(0.85~1.27)
rs528557(S2，跨膜) C vs. G 15 4 902/7 933 1.05(0.95~1.16) 0.340 61.0 RE 0.99(0.86~1.14)
rs2787094(V4，3′UTR) G vs. C 18 6 004/6 602 1.06(0.93~1.21) 0.380 66.0 RE 1.14(0.96~1.35)
rs44707(ST＋4，内含子) A vs. G 11 3 302/4 004 0.86(0.76~0.97) 0.020 52.0 RE 0.83(0.71~0.97)
图3 ADAM33 Met764Thr多态性的人群遗传学分析
图4 异质性贡献与效应影响Baujat式诊断
表3 哮喘异质性来源回归分析结果(rs3918396 A vs. G，k＝16，全模型I2＝38%，τ2＝0.011)
协变量 β(95%CI) P值 部分R2(%) 残差I2(%) VIF
种族(亚洲vs.其他) 0.21(0.04~0.38) 0.017 31.2 19 1.4
年龄(儿童vs.成人) 0.13(－0.02~0.28) 0.090 12.4 28 1.7
哮喘严重度(重度vs.轻中度) 0.11(－0.05~0.27) 0.170 9.1 31 1.5
对照来源(健康vs.过敏非哮喘) 0.06(－0.11~0.23) 0.490 3.2 35 1.2
样本量(log10) －0.08(－0.21~0.05) 0.230 6.5 33 1.3
发表年份(每1年) 0.03(－0.01~0.07) 0.150 7.8 32 1.6
研究质量(NOS评分) －0.04(－0.19~0.11) 0.610 1.8 36 1.1
LD(r2，与T2连锁强度) 0.17(0.01~0.33) 0.041 18.5 24 2.1
HWE偏离(P<0.05 vs.否) 0.15(－0.02~0.32) 0.080 10.3 30 1.4
多变量(种族＋年龄＋严重度) 见正文 0.031 42.7 18 <3
图5 rs3918396等位模型漏斗图(Egger P＝0.033)
图6 rs3918396 A风险等位基因频率分布
表4 敏感性与哮喘异质性来源Meta回归分析结果
结局指标 剔除单篇后汇总OR/MD波动范围 留一法I2变化 回归纳入协变量 协变量β(95%CI) 部分R2(%) 残差I2(%)
rs3918396哮喘易感性(等位模型) OR：1.14~1.22 38%→19%~29% 种族(亚洲vs.其他) 0.21(0.04~0.38) 31.2 19
rs3918396(显性模型，AA＋Aa vs. aa) OR：1.12~1.25 41%→24% 种族＋年龄 0.19(0.03~0.35) 38.5 21
rs2280090(T2)等位模型 OR：1.05~1.41 72%→48% 种族＋年龄＋严重度 0.26(0.06~0.46) 42.7 48
rs2280091(T1)等位模型 OR：0.96~1.18 78%→55% 种族＋对照来源 0.22(0.01~0.43) 29.4 52
rs511898(F＋1)等位模型 OR：1.09~1.31 45%→30% 种族＋儿童比例 0.18(0.02~0.34) 33.6 28
儿童哮喘(rs2280090) OR：1.08~1.52 44%→26% 种族＋HWE 0.24(0.05~0.43) 36.1 27
重度哮喘(rs511898 AA) OR：1.11~1.48 50%→33% 严重度＋对照来源 0.20(0.01~0.39) 30.5 34
FEV1/FVC(风险基因型vs.野生型，MD，%) MD：－3.10~－4.25 41%→27% 年龄＋测量方法 －0.42(－0.78~－0.06) 28.9 29
FEV1年下降(ml/年) MD：4.1~6.8 54%→38% 随访年限＋基线FEV1 1.05(0.32~1.78) 24.6 37
气道壁面积WA%(CT，MD，%) MD：1.35~2.04 55%→40% CT协议＋年龄 0.38(－0.05~0.81) 19.2 42
sADAM33水平(标准化MD) SMD：0.82~1.18 63%→45% 样本来源(BALF vs.血清) 0.31(0.08~0.54) 27.4 40
HDM-SLIT疗效(急性加重HR) HR：0.34~0.52 46%→31% 疗程＋基线嗜酸粒细胞 －0.28(－0.51~－0.05) 34.8 30
AIT后ACQ改善(MD，分) MD：0.28~0.55 39%→25% 治疗类型(SLIT vs. SCIT) 0.21(0.03~0.39) 30.1 28
ICS减量幅度(μg/d) MD：－50~－105 43%→29% 基线ICS剂量＋依从性 －0.26(－0.50~－0.02) 26.7 32
sIgG4升高(fold change, MD) MD：0.71~1.25 47%→33% 过敏原组分＋疗程 0.24(0.02~0.46) 29.0 33
抗IgE治疗后急性加重降幅 MD：－0.18~0.05 51%→44% 基线IgE＋体重 －0.09(－0.31~0.13) 8.5 46
1
龙铭，赵彦，高瞻，等. 新型药物在支气管哮喘中的临床应用与研究近况[J/OL]. 中华肺部疾病杂志(电子版), 2026, 19(3): 510-515.
2
Ganai I, Saha I, Banerjee P, et al. Insilico analysis of single nucleotide polymorphism (rs34377097)of TBXA2R gene and pollen induced bronchial asthma susceptibility in West Bengal population, India[J]. Front Immunol, 2023 Mar 1；14：1089514. https://doi.org/10.3389/fimmu.2023.1089514.
3
Global Initiative for Asthma. Global strategy for asthma management and prevention 2026[EB/OL]. 2026.

URL    
4
Kim SH, Pei QM, Jiang P, et al. Effect of active vitamin D3 on VEGF-induced ADAM33 expression and proliferation in human airway smooth muscle cells: implications for asthma treatment[J]. Respir Res, 2017, 18(1): 7.
5
Hur GY, Broide DH. Genes and pathways regulating decline in lung function and airway remodeling in asthma. Allergy Asthma Immunol Res. 2019 Sep；11(5)：604-621.
6
Buddhadev S, Prajapati B, Gadavala S, et al. Translating asthma pharmacogenomics into practice: evidence synthesis, clinical implementation, and future directions[J]. Asthma Allergy Immunol, 2026, 24(1): 13-25.
7
Zhou J, Bai W, Liu Q, et al. Silencing of ADAM33 restrains proliferation and induces apoptosis of airway smooth muscle cells in ovalbumin-induced asthma model[J]. J Cell Biochem, 2019, 120(2): 1435-1443.
8
Li HF, Yan LP, Wang K, et al. Association between ADAM33 polymorphisms and asthma risk: a systematic review and meta-analysis[J]. Respir Res, 2019, 20(1): 38.
9
Sultana Saheen, Banerjee Priyajit, Ganai Indranil, et al. Polymorphism in ADAM33 gene associated with asthmatics in West Bengal, India-An investigation by in-silico analysis[J]. World Allergy Organ J, 2023, 16(11): 100834.
10
Varricchi G, Ferri S, Pepys J, et al. Biologics and airway remodeling in severe asthma[J]. Allergy, 2022, 77(12): 3538-3552.
11
Kidoguchi M, Nagao M, Fukuoka A, et al. HLA-DPB1 allele associated with poor response to Japanese cedar pollen sublingual immunotherapy[J]. Allergy, 2022, 77(7): 2148-2157.
12
Page MJ, McKenzie JE, Bossuyt PM, et al. The PRISMA 2020 statement: an updated guideline for reporting systematic reviews[J]. BMJ, 2021, 372: n71.
13
Hunninghake GM, Lasky-Su J, Soto-Quiros ME, et al. Sex-stratified linkage analysis identifies a female-specific locus at 1p34 for asthma and induced sputum eosinophils[J]. Eur J Hum Genet, 2010, 18(2): 228-234.
14
Den Dekker HT, Duijts L, de Jongste JC, et al. Early growth and childhood asthma: a longitudinal study[J]. Eur Respir J, 2016, 47(5): 1398-1407.
15
van Eerdewegh P, Little RD, Josée D, et al. Association of the ADAM33 gene with asthma and bronchial hyperresponsiveness[J]. Nature, 2002, 418(6896): 426-430.
16
Schedel M, Depner M, Schoen C, et al. The role of polymorphisms in ADAM33, a disintegrin and metalloprotease 33, in childhood asthma and lung function in two German populations[J]. Respir Res, 2006, 7(1): 91.
17
Hunninghake GM, Gold DR.Sexual dimorphism: Is it relevant to steroid resistance or asthma control？[J]. J Allergy Clin Immunol, 2009, 124(4): 688-690.
18
Liang SQ, Wei X, Gong C, et al. A disintegrin and metalloprotease 33 (ADAM33) gene polymorphisms and the risk of asthma: a meta-analysis[J]. Hum Immunol, 2013, 74(5): 648-657.
19
Li LY, Spengler JD, Cao SJ. Prevalence of asthma and allergic symptoms in Suzhou, China: Trends by domestic migrant status[J]. J Expo Sci Environ Epidemiol, 2019, 29(4): 531-538.
20
Farjadian S, Moghtaderi M, Hoseini-Pouya BA, et al. ADAM33 gene polymorphisms in Southwestern Iranian patients with asthma[J]. Iran J Basic Med Sci, 2018, 21(8): 813-817.
21
Sultana S, Banerjee P, Ganai I, et al. Polymorphism in ADAM33 gene associated with asthmatics in West Bengal, India-An investigation by in-silico analysis[J]. World Allergy Organ J, 2023, 16(11): 100834.
22
de Jong K, Vonk JM, Timens W, et al. Genome-wide interaction study of gene-by-occupational exposure and effects on FEV1 levels[J]. J Allergy Clin Immunol, 2015, 136(6): 1664-1672.
23
Pedersen M, Liu S, Andersen ZJ, et al. Birth cohort studies of long-term exposure to ambient air pollution in early life and development of asthma in children and adolescents from denmark[J]. Res Rep Health Eff Inst, 2024, 2024(219): 1-63.
24
van der Valk RJP, Duijts L, Hijazi M, et al. An ADAM33 polymorphism associates with progression of preschool wheeze into childhood asthma: a prospective case-control study with replication in a birth cohort study[J]. Allergy, 2014, 69(4): 506-513.
25
Deng R, Zhao FY, Zhong XY. T1 polymorphism in a disintegrin and metalloproteinase 33 (ADAM33) gene may contribute to the risk of childhood asthma in Asians[J]. Inflamm Res, 2017, 66(5): 413-424.
26
Moffatt MF, Gut IG, Demenais F, et al. A large-scale, consortium-based genomewide association study of asthma[J]. N Engl J Med, 2010, 363(13): 1211-1221.
27
Sutherland ER, Goleva E, King TS, et al. Cluster analysis of obesity and asthma phenotypes[J]. PLoS One, 2012, 7(5): e36631.
28
Bogari NM, Amin AA, Rayes HH, et al. Next generation exome sequencing of pediatric asthma identifies rare and novelvariants in candidate genes[J]. Dis Markers, 2021, 8884229.
29
Kim SH. Biologic therapies in severe asthma and EGPA: targeted therapy and personalized care[J]. Tuberc Respir Dis, 2026, 89(1): 1-9.
30
Dennis T, Yuto H, Peter GG, et al. Diagnosis and treatment options for t2-low asthma[J]. J Allergy Clin Immunol Pract, 2025, 13(7): 1527-1539.
31
Agache I, Akdis CA. Endotypes and phenotypes of allergic diseases[J]. World Allergy Organ J, 2019, 12(7): 100066.
32
Sleziak J, Gawor A, Błazejewska M, et al. ADAM33’s role in asthma pathogenesis: an overview[J]. Int J Mol Sci, 2024, 25(4): 2318.
33
Balasubramanyam S, George EK, Wang E. Precision medicine and choosing a biologic in asthma: understanding the current state of knowledge for predictors of response and clinical remission[J]. Curr Opin Allergy Clin Immunol, 2025, 25(1): 66-74.
34
Liu T, Woodruff PG, Zhou X. Advances in non type 2 severe asthma：from molecular insights to novel treatment strategies[J]. Eur Respir J, 2024, 64(2): 2300826.
35
Global Initiative for Asthma. GINA 2025 pocket guide for asthma management and prevention[EB/OL]. 2025.

URL    
36
Laforce C, Albers F, Anna Danilewicz BS, et al. As-needed albuterol-budesonide in mild asthma[J]. N E J M, 2025, 393(2): 113-124.
37
Farjadian S, Moghtaderi M, Hoseini-Pouya BA, et al. ADAM33 gene polymorphisms in Southwestern Iranian patients with asthma[J]. Iran J Basic Med Sci, 2018, 21(8): 813-817.
38
苏冬菊，吕福祯，肖金玲，等. ADAM33基因多态性与尘螨过敏性哮喘易感性关系的研究[J]. 哈尔滨医科大学学报，2012, 46(5): 444-447.
39
王晶，龚新记. ADAM33基因与慢性气道疾病相关研究进展[J]. 新疆医科大学学报，2019, 42(8): 980-983.
40
向薇，方诗荣，谭荣，等. ADAM33基因在过氧化氢诱导的支气管上皮细胞凋亡及氧化损伤中的作用研究[J]. 中国免疫学杂志，2019, 35(8): 934-938.
41
常永莉，张莉媛，王惠琴，等. ADAM33基因T2位点多态性与支气管哮喘易感性的关联研究[J]. 检验医学与临床，2023, 20(1): 27-31.
42
Shally A, Priya T, Subramaniam G, et al. Association of ADAM33 gene polymorphisms with asthma in Indian children[J]. J Hum Genet, 2011, 56(3): 188-195.
43
GINA Executive Committee. Global Strategy for Asthma Management and Prevention (2024 update)[J]. Bethesda: NHLBI, 2024.
44
Wickman M, Bergström A, Lidegran M, et al. Sustained unresponsiveness after grass SLIT in children: a randomized, double-blind, placebo-controlled trial[J]. J Allergy Clin Immunol, 2019, 143(2): 895-899.e6.
45
王艺惠，都丽，任卉，等. ADAM33基因多态性在内蒙古中西部地区蒙古族与汉族的表达差异及其与COPD易感性的研究[J]. 内蒙古医科大学学报，2025, 47(4): 382-387.
46
朱淑芬，李建国. ADAM33基因多态性与蒙古族支气管哮喘的相关性[J]. 中华医学杂志，2016, 96(35): 2791-2795.
47
杨丽娟，邓高，丁波，等. ADAM33基因及其血清水平与广西壮族儿童哮喘发病风险分析[J]. 中国儿童保健杂志，2022, 30(11): 1185-1190.
48
李晓，张磊，汤昱，等. 从ADAM33基因T2位点多态性分析小儿支气管哮喘易感性及其严重程度的关系[J]. 中国中西医结合儿科学，2021, 13(1): 34-37.
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