期刊
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
卷 293, 期 2, 页码 F445-F455出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajprenal.00037.2007
关键词
transplantation; epithelial-to-mesenchymal transition; chronic allograft nephropathy; apoptosis; inflammation; heat shock proteins; hypoxia; blood oxygen level-dependent magnetic resonance imaging
资金
- NIDDK NIH HHS [DK067981-3] Funding Source: Medline
A major challenge for kidney transplantation is to dissect out the identifiable causes of chronic allograft tubulointerstitial fibrosis and to develop cause-specific treatment strategies. There has been a recent interest in the role of oxidative stress ( OS) as a mediator of injury in chronic allograft tubular atrophy ( TA) and interstitial fibrosis ( IF). A review of the literature and data from my laboratory studying chronic allograft TA/ IF in rat, rhesus monkey, and human kidneys suggests that OS is increased in graft- infiltrating macrophages, activated myofibroblasts, interstitium, and areas of tubular injury. Chronic allograft OS may be induced by inflammation, abnormal tissue oxygenation, immunosuppressant drugs, and comorbid clinical conditions including diabetes, hypertension, proteinuria, anemia, and dyslipidemia. Moreover, OS- induced chronic TA/ IF is associated with signaling pathways including inflammation, apoptosis, hypoxia, and epithelial- to- mesenchymal transition. Most of these injury pathways participate in a self- perpetuating cycle with OS. In conclusion, evidence suggests that OS is a common mechanism of injury in chronic allograft TA/ IF. However, most available data demonstrate a correlation and no causal relationship. Furthermore, the extent to which TA/ IF is dependent on OS is unknown. These questions may be answered by prospective randomized placebo- control trials examining the role of select antioxidants in the prevention of chronic allograft TA/ IF.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据