当前位置: X-MOL 学术Blood › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
A dastardly, deadly duo in stroke
Blood ( IF 20.3 ) Pub Date : 2020-02-06 , DOI: 10.1182/blood.2019004314
Shawn Jobe 1, 2
Affiliation  

CypD is a mitochondrial peptidylprolylisomerase. Its inhibitionordeletionabrogates the formation of a large inner mitochondrial membranepore knownas themitochondrial permeability transition pore (mPTP). Prolonged mPTP formation results in necrotic cell death, and pharmacologic agents that inhibit CypD and mPTP formation remain an interesting target for the prevention of cell death following ischemic injury.2 In platelets, CypD and mPTP formationmediate the transitionof an activated platelet from a classical aggregatory phenotype to a procoagulant phenotype.3 These procoagulant, or necrotic, platelets have distinct phenotypic and functional characteristics. Among these is the procoagulant platelet’s affinity for neutrophils, and their role in the initiation and formation of platelet/neutrophil aggregates.4

中文翻译:

一个卑鄙、致命的中风二人组

CypD 是一种线粒体肽基脯氨酰异构酶。它的抑制或缺失消除了称为线粒体通透性转换孔 (mPTP) 的大线粒体内膜孔的形成。延长的 mPTP 形成会导致坏死细胞死亡,抑制 CypD 和 mPTP 形成的药物仍然是预防缺血性损伤后细胞死亡的有趣目标。 2 在血小板中,CypD 和 mPTP 形成介导了活化血小板从经典聚集表型的转变3 这些促凝或坏死的血小板具有不同的表型和功能特征。其中包括促凝血血小板对中性粒细胞的亲和力,以及它们在血小板/中性粒细胞聚集体的起始和形成中的作用。 4
更新日期:2020-02-06
down
wechat
bug