Apoptosis of leukocytes: Basic concepts and implications in uremia
Apoptosis of leukocytes: Basic concepts and implications in uremia
复制标题
DOI：
10.1046/j.1523-1755.2001.59780197.x
复制
发表时间：
2001-02-01
影响因子：
19.6
通讯作者：
Pereira, BJG
中科院分区：
文献类型：
--
作者：
Jaber, BL;Cendoroglo, M;Pereira, BJG
循环血液白细胞具有短的预期寿命，并且通过进行程序性细胞死亡或凋亡来结束它们的生命。细胞凋亡是细胞死亡的一种活跃形式，由许多刺激引发，并受到复杂的调节。过量和减少量的细胞凋亡具有病理学意义。有证据表明，细胞凋亡可能在尿毒症免疫功能障碍的病理生理学中发挥作用。事实上，在慢性肾衰竭患者的淋巴细胞、单核细胞和多形核白细胞中观察到了加速的程序性细胞死亡。这可能部分是由于尿毒症毒素的保留。本文的目的是审查加速白细胞凋亡的证据，关键的调节凋亡途径，以及这种高度组织化的过程中可能发挥的作用，在尿毒症免疫功能障碍的发病机制。
Circulating blood leukocytes have short life expectancies and end their lives by committing programmed cell death or apoptosis. Apoptosis is an active form of cell death that is initiated by a number of stimuli and is intricately regulated. Apoptosis in both excessive and reduced amounts has pathological implications. Evidence suggests that apoptosis may play a role in the pathophysiology of immune dysfunction in uremia. Indeed, accelerated programmed cell death has been observed in lymphocytes, monocytes, and polymorphonuclear leukocytes among patients with chronic renal failure. This may be due in part to the retention of uremic toxins. The aim of this article is to review the evidence for accelerated leukocyte apoptosis, key regulatory apoptotic pathways, and the possible role of this highly organized process in the pathogenesis of immune dysfunction in uremia.