Study on Correlation of Serum lncRNA MALAT1 Level with Markers of Myocardial Injury and Coagulation Function in Patients with Acute Myocardial Infarction
WANG Xing, HU Ya-hong
The First Affiliated Hospital of Xi'an Jiaotong University,Xi'an Shaanxi 710061
Abstract:【Objective】To detect the expression level of long non-coding RNA-lung adenocarcinoma metastasis-associated transcription factor 1 (IncRNA MALAT1) in serum of patients with acute myocardial infarction and analyze its relationships with marks of myocardial injury and coagulation function in actual myocardial infarction (AMI). 【Methods】A total of 103 patients with acute myocardial infarction admitted to our hospital from January 2017 to January 2019 were selected as the observation group, and 103 healthy volunteers who were examined in our hospital during the same period were selected as the control group. The level of lncRNA MALAT1 in serum was detected by qRT-PCR and the levels of myocardial injury markers and coagulation factors were detected by ELISA. The correlations of the level of lncRNA MALAT1 with myocardial injury and coagulation function were analyzed. 【Results】The levels of NT-proBNP, CK-MB, CK, cTnI, MYO, coagulation indexes such as PT, APTT, INR, FIB, vWF, PAI-1 and serum lncRNA MALAT1 in acute myocardial infarction group were significantly higher than those in healthy control group (all P<0.05), while the values of PT, APTT and INR were lower than those in the control group, and the differences were statistically significant. (P<0.05). Serum lncRNA MALAT1 was positively correlated with NT-proBNP, CK-MB, cTnI, vWF and PAI-1 in patients with acute myocardial infarction (P<0.05), and IncRNA MALAT1 level was negatively correlated with PT and APTT (P<0.05). High NT-proBNP level, high CK-MB level, low APTT level, high vWF level and high lncRNA MALAT1 level were risk factors for acute myocardial infarction (all P<0.05). 【Conclusion】The expression level of serum lncRNA MALAT1 of patients with acute myocardial infarction was significantly increased, which may promote the occurrence of acute myocardial infarction by influencing the changes of myocardial markers and coagulation indexes.
王星, 胡亚红. 急性心肌梗死患者血清lncRNA MALAT1水平与心肌损伤标志物、凝血功能指标的相关性研究[J]. 医学临床研究, 2022, 39(4): 553-556.
WANG Xing, HU Ya-hong. Study on Correlation of Serum lncRNA MALAT1 Level with Markers of Myocardial Injury and Coagulation Function in Patients with Acute Myocardial Infarction. JOURNAL OF CLINICAL RESEARCH, 2022, 39(4): 553-556.
[1] 董志华,张川海,赵赫.灯盏花素注射液联合比伐芦定对急性心肌梗死患者PCI术后心电图指标及心功能的影响[J].医学临床研究,2021,38(2):233-236.
[2] 张小路, 杜梅红. LncRNA MALAT1调控miR-204表达影响胰腺癌细胞的生物学行为[J].中国肿瘤生物治疗杂志, 2018, 25(1):79-84.
[3] 陈凤惟, 张成, 董慧, 等. 慢性间歇低氧上调心肌lncRNA MALAT1及相关分子的表达[J].中国呼吸与危重监护杂志, 2018, 17(4):377-382.
[4] HUANG S.Long noncoding RNA MALAT1 mediates cardiac fibrosis in experimental postinfarct myocardium mice model[J].J Cell Physiol,2019, 1(9):234-246.
[5] 高瑜, 闫旭, 张会君. 急性心肌梗死患者症状典型性与院前延误的关系[J].中国老年学杂志, 2014, 34(23):6592-6593.
[6] ZHANG M, GU H, XU W, et al. Down-regulation of lncRNA MALAT1 reduces cardiomyocyte apoptosis and improves left ventricular function in diabetic rats[J].Int J Cardiol,2016, 203(1):214-216.
[7] LI Q, ZHU W, ZHANG B, et al. The MALAT1 gene polymorphism and its relationship with the onset of congenital heart disease in Chinese[J].Biosci Rep,2018, 38(3):1-7.
[8] 张鸿雁, 李艳芳, 吕靖, 等. 老年性舒张性心力衰竭患者血清NT-ProBNP、hs-CRP、cTnI水平及预后的关系[J].实用医学杂志, 2011, 27(21):3901-3902.
[9] SUN Z, WU W, LIU J, et al. Influence of glucose-lowering rate on CK-MB and myoglobin serum levels in type-2 diabetes patients with coronary heart disease[J].Hum Immunol,2014, 75(12):1182-1187.
[10] FAN J B, MA J, XIA N,et al.Clinical value of combined detection of CK-MB, MYO, cTnI and plasma NT-proBNP in diagnosis of acute myocardial infarction[J].Clin Lab,2017, 63(3): 427-433.
[11] 刘晓霞, 亢瑞娜. 冠心病患者血浆纤维蛋白原、活化部分凝血酶时间、凝血酶原时间及血清Ca2+水平的临床研究[J].现代预防医学, 2012, 39(14):3725-3727.
[12] MICHALIK K M, YOU X, MANAVSKI Y, et al. Long noncoding rna MALAT1 regulates endothelial cell function and vessel growthnovelty and significance[J].Circ Res,2014, 114(9):1389-1397.