Ischemia and reperfusion--from mechanism to translation.
Ischemia and reperfusion--from mechanism to translation.
复制标题
缺血和再灌注 - 从翻译机构。
作者：
缺血和再灌注引起的组织损伤导致多种病理学的发病率和死亡率，包括心肌梗死、缺血性卒中、急性肾损伤、创伤、循环停止、镰状细胞病和睡眠呼吸暂停。缺血再灌注损伤也是器官移植和心胸、血管和普通外科手术中的主要挑战。缺血器官内代谢供需失衡导致严重的组织缺氧和微血管功能障碍。随后的再灌注进一步增强了先天性和适应性免疫应答以及细胞死亡程序的激活。了解缺血和再灌注的分子和免疫学后果的最新进展可能导致治疗缺血和再灌注相关组织炎症和器官功能障碍患者的创新治疗策略。
Ischemia and reperfusion–elicited tissue injury contributes to morbidity and mortality in a wide range of pathologies, including myocardial infarction, ischemic stroke, acute kidney injury, trauma, circulatory arrest, sickle cell disease and sleep apnea. Ischemia-reperfusion injury is also a major challenge during organ transplantation and cardiothoracic, vascular and general surgery. An imbalance in metabolic supply and demand within the ischemic organ results in profound tissue hypoxia and microvascular dysfunction. Subsequent reperfusion further enhances the activation of innate and adaptive immune responses and cell death programs. Recent advances in understanding the molecular and immunological consequences of ischemia and reperfusion may lead to innovative therapeutic strategies for treating patients with ischemia and reperfusion–associated tissue inflammation and organ dysfunction.
登录
查看更多内容
影响因子：
56.9
作者：
Blackstone, E;Morrison, M;Roth, MB
通讯作者：
Roth, MB
影响因子：
4.8
作者：
Daniels, Isadora Susan;Zhang, Jianfa;Lee, Cheng Chi
通讯作者：
Lee, Cheng Chi
DOI：
10.1152/ajpheart.00472.2006
发表时间：
2006-11-01
影响因子：
4.8
作者：
Eckle, Tobias;Grenz, Almut;Eltzschig, Holger K.
通讯作者：
Eltzschig, Holger K.
影响因子：
20.3
作者：
Eckle, Tobias;Faigle, Marion;Eltzschig, Holger K.
通讯作者：
Eltzschig, Holger K.
DOI：
10.1073/pnas.97.19.10526
发表时间：
2000-09-12
影响因子：
11.1
作者：
Brines, ML;Ghezzi, P;Cerami, A
通讯作者：
Cerami, A