The involvement of oxidative stress in the progression of renal injury
The involvement of oxidative stress in the progression of renal injury
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DOI：
10.1159/000014377
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发表时间：
1999-01-01
影响因子：
3
通讯作者：
Nath, KA
中科院分区：
文献类型：
--
作者：
Haugen, E;Nath, KA
活性氧参与进行性肾损伤得到了以下几方面证据的支持：慢性肾损伤中氧化剂的生成增加;各种抗氧化剂策略在慢性肾损伤模型中发挥有益作用;氧化应激可诱导未处理肾脏发生类似于慢性肾病中所见的变化。氧化剂可能通过其肾脏血液动力学作用、损害肾小球选择性透过性、诱导过度或异常生长反应、诱导细胞表型丧失和细胞凋亡以及最终促进急性和慢性炎症反应而导致进行性肾病。某些粘附分子和促炎介质以及转录因子NF κ B B可被氧化剂上调。氧化剂也可以诱导纤维化细胞因子TGF β 1，这是一种广泛参与进行性肾损伤的细胞因子。通过饮食或药物方法减少肾氧化应激为针对延缓进行性肾损伤的治疗提供了有吸引力的靶点。
That reactive oxygen species are involved in progressive renal injury is supported by several lines of evidence: increased generation of oxidants occurs in chronic renal injury; various antioxidant strategies exert beneficial effects in models of chronic renal injury; and, oxidative stress can induce changes in the otherwise unmanipulated kidney that resemble those seen in chronic renal disease. Oxidants may contribute to progressive renal disease by virtue of their renal haemodynamic actions, by impairing glomerular permselective properties, by inducing inordinate or aberrant growth responses, by inducing loss of cellular phenotype and apoptosis, and finally, by promoting acute and chronic inflammatory responses. Certain adhesion molecules and proinflammatory mediators, and the transcription factor NF kappa B, can be upregulated by oxidants. Oxidants can also induce the fibrogenic cytokine, TGF beta 1, one that is widely incriminated in progressive renal injury. Reduction in renal oxidative stress by dietary or pharmacologic approaches provides an appealing target for therapies directed towards the retardation of progressive renal injury.