Liberale Luca, Bonaventura Aldo, Montecucco Fabrizio
Center for Molecular Cardiology, University of Zürich, Schlieren 8952, Switzerland.
First Clinic of Internal Medicine, Department of Internal Medicine, University of Genoa, Genoa 16132, Italy.
World J Cardiol. 2018 Oct 26;10(10):123-126. doi: 10.4330/wjc.v10.i10.123.
Immune system activation and dysfunction characterize the early phase of reperfusion after a myocardial infarction (MI). Despite initially neglected, adaptive immunity has been recently showed to play an important role in this setting. In fact, the immune system can recognize sequestered antigens released by the necrotic tissue, initiating a deleterious autoimmune vicious circle leading to worse outcome. In their recent work, Angelini et al shed the light on a new feature of post-MI which involves two "old players" of post-ischemic myocardial injury: CD31 and matrix metalloproteinase (MMP)-9. Specifically, the authors showed that an enhancement of MMP-9 release could determine the cleavage of inhibitory CD31 from CD4+ T-cells surface in patients with Acute Coronary Syndromes (ACS). These findings open the room for new studies investigating the role of MMP9 in other pathological processes associated with a reduction of CD31 functionality, such as plaque instability and rupture. Of interest, in the case of a causative role for CD31 shedding in ACS would be confirmed, there might be a potential role for the administration of CD31 protein or analogue compounds to blunt post-ischemic cardiac inflammation and improve ACS outcome.
免疫系统激活和功能障碍是心肌梗死（MI）后再灌注早期的特征。尽管适应性免疫最初被忽视，但最近研究表明其在这种情况下发挥重要作用。事实上，免疫系统能够识别坏死组织释放的隔离抗原，引发有害的自身免疫恶性循环，导致更糟的结果。在最近的研究中，安杰利尼等人揭示了心肌梗死后的一个新特征，该特征涉及缺血后心肌损伤的两个“老参与者”：CD31和基质金属蛋白酶（MMP）-9。具体而言，作者表明，在急性冠状动脉综合征（ACS）患者中，MMP-9释放增强可导致CD4+T细胞表面抑制性CD31的裂解。这些发现为新的研究开辟了空间，这些研究将探讨MMP9在其他与CD31功能降低相关的病理过程中的作用，如斑块不稳定和破裂。有趣的是，如果CD31脱落在ACS中起因果作用得到证实，那么给予CD31蛋白或类似化合物以减轻缺血后心脏炎症并改善ACS结局可能具有潜在作用。
