Correlation of serum miR‑210, TSG‑6 and CTRP3 with myocardial fibrosis and prognosis in patients with dilated cardiomyopathy
Received date: 2025-09-09
Online published: 2025-12-18
目的 探讨血清微小RNA-210(miR-210)、肿瘤坏死因子α刺激基因6(TSG-6)、补体C1q肿瘤坏死因子相关蛋白3(CTRP3)与扩张型心肌病(DCM)患者心肌纤维化及预后的相关性。 方法 选取2024年3—8月泰州市人民医院收治的117例DCM患者(DCM组)。根据DCM患者心脏磁共振检查,分为纤维化组(n = 96)和非纤维化组(n = 21)。根据DCM患者1年内预后随访是否发生急性心力衰竭,分为心衰组(n = 47)和非心衰组(n = 70)。同期选取58例健康志愿者(健康对照组)。比较各组血清miR-210、TSG?6、CTRP3、Ⅲ型前胶原N端肽(PⅢNP)、左室射血分数(LVEF)、N末端B型利钠肽(NT-proBNP)。 结果 DCM组血清miR-210、TSG-6、PⅢNP、NT-proBNP水平高于健康对照组,CTRP3、LVEF低于健康对照组(P < 0.05)。纤维化组血清miR-210、TSG-6、PⅢNP、NT-proBNP水平高于非纤维化组,CTRP3、LVEF低于非纤维化组(P < 0.05)。心衰组血清miR-210、TSG-6、PⅢNP、NT-proBNP水平高于非心衰组,CTRP3、LVEF低于非心衰组(P < 0.05)。血清miR-210、TSG-6水平与血清PⅢNP、NT-proBNP水平呈正相关(P < 0.05),与LVEF呈负相关(P < 0.05)。血清miR-210高水平(OR = 2.065,95%CI = 1.116 ~ 3.821)、TSG-6高水平(OR = 1.047,95%CI = 1.013 ~ 1.083)是DCM患者发生心衰的危险因素(P < 0.05),而血清CTRP3高水平(OR = 0.911,95%CI = 0.849 ~ 0.978)是保护性因素(P < 0.05)。血清miR-210、TSG?6、CTRP3预测DCM患者发生心衰的灵敏度分别为72.34%、74.47%、74.47%,特异度分别为62.86%、62.86%、68.57%(AUC = 0.669,AUC = 0.712,AUC = 0.759)。 结论 DCM患者血清miR-210、TSG-6上调,CTRP3下调,并且与心肌纤维化和心功能密切相关。miR-210、TSG-6、CTRP3对DCM预后有较好的预测价值。
关键词: 扩张型心肌病; 心肌纤维化; 预后; 微小RNA?210; 肿瘤坏死因子α刺激基因6; 补体C1q肿瘤坏死因子相关蛋白3
王叶宝 , 林永萍 , 刘玲 , 李建民 . 血清miR-210、TSG-6、CTRP3水平与扩张型心肌病患者心肌纤维化及预后的关系[J]. 实用医学杂志, 2025 , 41(23) : 3690 -3696 . DOI: 10.3969/j.issn.1006-5725.2025.23.009
Objective To investigate the correlation between serum microRNA-210 (miR-210), tumor necrosis factor-stimulated gene 6 (TSG-6), and complement C1q tumor necrosis factor-related protein 3 (CTRP3) and their association with myocardial fibrosis and prognosis in patients with dilated cardiomyopathy (DCM). Methods A total of 117 patients with DCM admitted to Taizhou People's Hospital between March and August 2024 were enrolled in the DCM group. Based on cardiac magnetic resonance imaging findings, these patients were further classified into a myocardial fibrosis group (n = 96) and a non-fibrosis group (n = 21). Additionally, according to the occurrence of acute heart failure during one-year follow-up, they were categorized into a heart failure group (n = 47) and a non-heart failure group (n = 70). Concurrently, 58 age- and sex-matched healthy volunteers were recruited as the control group. Serum levels of miR-210, TSG-6, CTRP3, N-terminal propeptide of type Ⅲ procollagen (PⅢNP), left ventricular ejection fraction (LVEF), and N-terminal pro-B-type natriuretic peptide (NT-proBNP) were measured and compared across all groups. Results The DCM group exhibited significantly higher serum levels of miR-210, TSG-6, PⅢNP, and NT-proBNP, lower CTRP3 levels, and reduced LVEF compared to the healthy controls (P < 0.05). Similarly, the fibrosis group showed elevated serum levels of miR-210, TSG-6, PⅢNP, and NT-proBNP, decreased CTRP3 levels, and impaired LVEF relative to the non-fibrosis group (P < 0.05). The heart failure group also demonstrated higher serum concentrations of these biomarkers, along with lower CTRP3 and reduced LVEF, compared to the non-heart failure group (P < 0.05). Serum miR-210 and TSG-6 levels were positively correlated with PⅢNP and NT-proBNP (P < 0.05) and negatively correlated with LVEF (P < 0.05). Multivariate analysis revealed that elevated serum miR-210 (OR = 2.065, 95%CI: 1.116 ~ 3.821) and TSG-6 (OR = 1.047, 95%CI: 1.013 ~ 1.083) were independent risk factors for heart failure in DCM patients (P < 0.05), whereas higher CTRP3 levels (OR = 0.911, 95%CI: 0.849 ~ 0.978) were associated with a protective effect (P < 0.05). The sensitivity of serum miR-210, TSG-6, and CTRP3 in predicting heart failure in DCM patients was 72.34%, 74.47%, and 74.47%, respectively, with specificities of 62.86%, 62.86%, and 68.57%, yielding AUC values of 0.669, 0.712, and 0.759, respectively. Conclusions Serum levels of miR-210 and TSG-6 are elevated, whereas CTRP3 levels are reduced in patients with DCM. These biomarkers are closely associated with myocardial fibrosis and cardiac function impairment. Moreover, miR-210, TSG-6, and CTRP3 exhibit significant predictive value for the prognosis of DCM.
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