Endothelial microvesicles in hypoxic hypoxia diseases.

Endothelial microvesicles in hypoxic hypoxia diseases.
复制标题

DOI:
10.1111/jcmm.13671
复制
发表时间:
2018-08
影响因子:
5.3
通讯作者:
Zhang L
Zhang L
中科院分区:
医学2区
文献类型:
--
作者:
Deng F;Wang S;Xu R;Yu W;Wang X;Zhang L

文献摘要

参考文献

被引文献

相似文献

低氧缺氧包括吸入氧分压异常低、外部呼吸功能障碍引起的呼吸缺氧和静脉血流入动脉血,其特征是动脉氧分压降低,导致组织缺氧。具体特征包括动脉氧分压和氧含量降低。低氧性低氧疾病(hhd)因其高发病率和死亡率而受到越来越多的关注,越来越多的证据表明,缺氧诱导的氧化应激、凝血、炎症和血管生成在hhd相关血管内皮损伤的生理和病理过程中起着极其重要的作用。有趣的是,内皮微泡(emv)可由缺氧、缺氧诱导的氧化应激、凝血和HHDs炎症诱导,已成为细胞间通讯和细胞功能的关键介质。从活化或凋亡的内皮细胞(ECs)脱落的emv反映了ECs损伤的程度,emv水平升高存在于几种HHDs中,包括阻塞性睡眠呼吸暂停综合征和慢性阻塞性肺疾病。此外,emv具有促凝、促炎和血管生成功能,影响HHDs的病理过程。本文综述了emv在HHDs的诊断、分期、治疗和临床预后中的新作用。
Hypoxic hypoxia, including abnormally low partial pressure of inhaled oxygen, external respiratory dysfunction‐induced respiratory hypoxia and venous blood flow into the arterial blood, is characterized by decreased arterial oxygen partial pressure, resulting in tissue oxygen deficiency. The specific characteristics include reduced arterial oxygen partial pressure and oxygen content. Hypoxic hypoxia diseases (HHDs) have attracted increased attention due to their high morbidity and mortality and mounting evidence showing that hypoxia‐induced oxidative stress, coagulation, inflammation and angiogenesis play extremely important roles in the physiological and pathological processes of HHDs‐related vascular endothelial injury. Interestingly, endothelial microvesicles (EMVs), which can be induced by hypoxia, hypoxia‐induced oxidative stress, coagulation and inflammation in HHDs, have emerged as key mediators of intercellular communication and cellular functions. EMVs shed from activated or apoptotic endothelial cells (ECs) reflect the degree of ECs damage, and elevated EMVs levels are present in several HHDs, including obstructive sleep apnoea syndrome and chronic obstructive pulmonary disease. Furthermore, EMVs have procoagulant, proinflammatory and angiogenic functions that affect the pathological processes of HHDs. This review summarizes the emerging roles of EMVs in the diagnosis, staging, treatment and clinical prognosis of HHDs.
FAM3A 通过激活 Akt 存活通路、抑制炎症和氧化应激介导 PPAR gamma 对肝脏缺血再灌注损伤的保护作用
DOI: 10.18632/oncotarget.17805
发表时间: 2017-07-25
期刊: Oncotarget
影响因子: --
作者:
Chen Z;Wang J;Yang W;Chen J;Meng Y;Geng B;Cui Q;Yang J
通讯作者: Yang J
DOI: 10.1183/09031936.00107408
发表时间: 2009-03-01
影响因子: 24.3
作者:
Ayers, L.;Ferry, B.;Kohler, M.
通讯作者: Kohler, M.
DOI: 10.1378/chest.10-2223
发表时间: 2011-08-01
期刊: CHEST
影响因子: 9.6
作者:
Drager, Luciano F.;Polotsky, Vsevolod Y.;Lorenzi-Filho, Geraldo
通讯作者: Lorenzi-Filho, Geraldo
DOI: 10.1160/th13-12-1006
发表时间: 2014-09-01
影响因子: 6.7
作者:
Campello, Elena;Spiezia, Luca;Simioni, Paolo
通讯作者: Simioni, Paolo
DOI: 10.1016/j.acvd.2010.06.005
发表时间: 2010-06-01
影响因子: 3
作者:
Bal, Laurence;Ederhy, Stephane;Cohen, Ariel
通讯作者: Cohen, Ariel