肿瘤坏死因子受体3相互作用蛋白2与心房颤动相关性的临床研究

Study on the association between TRAF3IP2 and atrial fibrillation

目的探讨肿瘤坏死因子受体3相互作用蛋白2(TRAF3IP2)与心房颤动(下称房颤)的相关性。方法选择南京医科大学附属淮安第一医院2021年6至12月收治的瓣膜性心脏病患者41例,根据是否合并房颤分为房颤组22例和非房颤组19例。收集患者的临床资料、全血以及部分心房肌组织,比较两组患者TRAF3IP2表达水平和纤维化指标[胶原和α平滑肌肌动蛋白(α-SMA)含量]。结果房颤组左心房直径(LAD)、TRAF3IP2表达水平均高于非房颤组(均P<0.01),TRAF3IP2表达与LAD呈直线相关(r=0.33,P=0.037)。分层分析显示在LAD≤3.5 mm的患者中,房颤组TRAF3IP2表达水平高于非房颤组;在LAD>3.5 mm的患者中,房颤组TRAF3IP2表达水平高于非房颤组(均P<0.01)。马松染色和免疫组化染色显示,房颤组心房肌胶原含量及TRAF3IP2表达水平高于非房颤组。Western blotting结果显示房颤组心房肌组织TRAF3IP2和α-SMA表达水平高于非房颤患者。结论TRAF3IP2与房颤存在相关性,具体表现为房颤患者的TRAF3IP2表达水平高于非房颤患者,提示TRAF3IP2可能参与房颤的进展。

Objective To evaluate the association of TRAF3IP2 with atrial fibrillation(AF).Methods A total of 41 patients experiencing valvular heart diseases who were admitted to the Affiliated Huaian No.1 People's Hospital of Nanjing Medical University from June to December 2021 were enrolled,and they were divided into AF group(n=22)and non-AF group(n=19)based on whether AF was existed.Clinical data,whole blood and left atrial tissues of patients were collected.Then we analyzed the TRAF3IP2 levels and the degree of fibrosis(the content of collagen andα-SMA)of patients in the two groups.Results The left atrial diameters(LAD)and the expressions of TRAF3IP2 in AF group were significantly higher than those of non-AF group(both P<0.01).Besides,TRAF3IP2 expressions were linearly associated with the LAD(r=0.33,P=0.037).Stratified analysis showed that the TRAF3IP2 expressions were higher in AF group than non-AF group not only in patients with LAD≤3.5 mm but also in patients with LAD>3.5 mm(both P<0.01).The Masson and immunohistological staining showed that levels of collagen content and TRAF3IP2 expression in AF group were higher than those in non-AF group,while Western blotting analysis suggested the expressions of TRAF3IP2 andα-SMA were higher in AF than in non-AF group.Conclusion Our data demonstrated an association between TRAF3IP2 and AF that the expressions of TRAF3IP2 in AF patients were higher than those in non-AF subjects,indicating an involvement of TRAF3IP2 in AF progression.