西班牙国家心血管研究中心Pilar Martín团队研究了一种检测急性心肌炎的新型循环MicroRNA。2021年5月26日，该研究发表在《新英格兰医学杂志》上。

急性心肌炎的诊断通常需要心肌内膜活检（有创）或心血管磁共振成像（非普遍可用）。因此需要更多的诊断方法。研究组试图找出一种新型microRNA诊断急性心肌炎。

为了鉴定一种针对心肌炎的microRNA，研究组在诱导小鼠实验性自身免疫性心肌炎或心肌梗死后，对分类的CD4+T细胞和17型辅助性T（Th17）细胞进行microRNA微阵列分析和定量聚合酶链反应（qPCR）分析。研究组还对柯萨奇病毒诱导的小鼠心肌炎样本进行了qPCR。然后他们鉴定了这种microRNA的人类同源物，并将其在急性心肌炎患者血浆中的表达与不同对照组的表达进行了比较。

研究组证实Th17细胞是心肌炎急性期心肌损伤的特征性细胞，其特征是产生白细胞介素-17。microRNA mmu-miR-721由Th17细胞合成，存在于急性自身免疫性或病毒性心肌炎小鼠血浆中，而在急性心肌梗死小鼠血浆中不存在。人类同源物，命名为hsa-miR-Chr8:96，在四个独立的心肌炎患者队列中鉴定。这种新型microRNA区分急性心肌炎和心肌梗死患者的受试者操作特征曲线下面积为0.927。在校正了年龄、性别、射血分数和血清肌钙蛋白水平后，microRNA在模型中保留了其诊断价值。

总之，在小鼠和心肌炎患者中鉴定出一种新型microRNA后，研究组发现人类同源物（hsa-miR-Chr8:96）可用于区分心肌炎患者和心肌梗死患者。

附：英文原文

Title: A Novel Circulating MicroRNA for the Detection of Acute Myocarditis

Author: Rafael Blanco-Domínguez, M.Sc.,, Raquel Sánchez-Díaz, Ph.D.,, Hortensia de la Fuente, M.D., Ph.D.,, Luis J. Jiménez-Borreguero, M.D.,, Adela Matesanz-Marín, Ph.D.,, Marta Relao, Ph.D.,, Rosa Jiménez-Alejandre, M.Sc.,, Beatriz Linillos-Pradillo, M.Sc.,, Katerina Tsilingiri, Ph.D.,, María L. Martín-Mariscal, M.D.,, Laura Alonso-Herranz, Ph.D.,, Guillermo Moreno, M.Sc.,, Roberto Martín-Asenjo, M.D.,, Marcos M. García-Guimaraes, M.D.,, Katelyn A. Bruno, Ph.D.,, Esteban Dauden, M.D., Ph.D.,, Isidoro González-álvaro, M.D., Ph.D.,, Luisa M. Villar-Guimerans, M.D., Ph.D.,, Amaia Martínez-León, M.D.,, Ane M. Salvador-Garicano, Ph.D.,, Sam A. Michelhaugh, B.A.,, Nasrien E. Ibrahim, M.D.,, James L. Januzzi, M.D.,, Jan Kottwitz, M.D.,, Sabino Iliceto, M.D.,, Mario Plebani, M.D.,, Cristina Basso, M.D., Ph.D.,, Anna Baritussio, M.D., Ph.D.,, Mara Seguso, M.Sc.,, Renzo Marcolongo, M.D.,, Mercedes Ricote, Ph.D.,, DeLisa Fairweather, Ph.D.,, Héctor Bueno, M.D., Ph.D.,, Leticia Fernández-Friera, M.D., Ph.D.,, Fernando Alfonso, M.D., Ph.D.,, Alida L.P. Caforio, M.D., Ph.D.,, Domingo A. Pascual-Figal, M.D., Ph.D.,, Bettina Heidecker, M.D., Ph.D.,, Thomas F. Lüscher, M.D., Ph.D.,, Saumya Das, M.D., Ph.D.,, Valentín Fuster, M.D., Ph.D.,, Borja Ibáez, M.D., Ph.D.,, Francisco Sánchez-Madrid, Ph.D.,, and Pilar Martín, Ph.D.

Issue&Volume: 2021-05-26

Abstract:

Background

The diagnosis of acute myocarditis typically requires either endomyocardial biopsy (which is invasive) or cardiovascular magnetic resonance imaging (which is not universally available). Additional approaches to diagnosis are desirable. We sought to identify a novel microRNA for the diagnosis of acute myocarditis.

Methods

To identify a microRNA specific for myocarditis, we performed microRNA microarray analyses and quantitative polymerase-chain-reaction (qPCR) assays in sorted CD4+ T cells and type 17 helper T (Th17) cells after inducing experimental autoimmune myocarditis or myocardial infarction in mice. We also performed qPCR in samples from coxsackievirus-induced myocarditis in mice. We then identified the human homologue for this microRNA and compared its expression in plasma obtained from patients with acute myocarditis with the expression in various controls.

Results

We confirmed that Th17 cells, which are characterized by the production of interleukin-17, are a characteristic feature of myocardial injury in the acute phase of myocarditis. The microRNA mmu-miR-721 was synthesized by Th17 cells and was present in the plasma of mice with acute autoimmune or viral myocarditis but not in those with acute myocardial infarction. The human homologue, designated hsa-miR-Chr8:96, was identified in four independent cohorts of patients with myocarditis. The area under the receiver-operating-characteristic curve for this novel microRNA for distinguishing patients with acute myocarditis from those with myocardial infarction was 0.927 (95% confidence interval, 0.879 to 0.975). The microRNA retained its diagnostic value in models after adjustment for age, sex, ejection fraction, and serum troponin level.

Conclusions

After identifying a novel microRNA in mice and humans with myocarditis, we found that the human homologue (hsa-miR-Chr8:96) could be used to distinguish patients with myocarditis from those with myocardial infarction.

DOI: 10.1056/NEJMoa2003608

Source: https://www.nejm.org/doi/full/10.1056/NEJMoa2003608