Infarcted Myocardium Calls for T-Cell Help to Regulate Repair.

Infarcted Myocardium Calls for T-Cell Help to Regulate Repair.
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梗塞心肌需要 T 细胞帮助调节修复。

DOI:
10.1161/circresaha.123.322556
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发表时间:
2023
影响因子:
20.1
通讯作者:
Alcaide,Pilar
Alcaide,Pilar
中科院分区:
医学1区
文献类型:
--
作者:
Li,Xudong;Alcaide,Pilar

文献摘要

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全球有超过1.2亿人罹患缺血性心脏病。损伤部位的细胞死亡触发免疫和纤维化反应,共同作用形成心脏修复不可或缺的疤痕。免疫细胞动员到损伤部位是修复所必需的,但在瘢痕形成后,心脏免疫格局发生变化,这些变化最终对慢性缺血性心脏病的心脏收缩能力产生负面影响。1了解在协调的心脏修复反应中相互作用的新的免疫学机制对于发现治疗缺血性心脏病的新的免疫调节疗法是至关重要的。
Ischemic heart disease affects over 120 million peo-ple worldwide. Cell death at the injury site triggers an immune and fibrotic response that work in tandem to form an indispensable scar for cardiac repair. Immune cell mobilization to the site of injury is necessary for repair, but the cardiac immune landscape changes after the scar formation and these alterations end up negatively impacting cardiac contractility in chronic ischemic heart disease. 1 Understanding novel immunological mechanisms that interplay during the coordinated cardiac repair response is of utmost importance to discover new immunomodulatory therapeutics for ischemic heart disease.