Reactive oxygen species as the molecular modulators of calcium oxalate kidney stone formation: evidence from clinical and experimental investigations.
Reactive oxygen species as the molecular modulators of calcium oxalate kidney stone formation: evidence from clinical and experimental investigations.
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DOI：
10.1016/j.juro.2012.05.078
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发表时间：
2013-03
期刊：
影响因子：
--
通讯作者：
Khan SR
中科院分区：
文献类型：
--
作者：
Khan SR
特发性草酸钙肾结石在附着于兰德尔斑块（肾乳头表面上皮下沉积物）时形成。人们对斑块形成和生长机制知之甚少。身体其他部位的斑块形成是由活性氧和氧化应激引发的。本综述探讨了活性氧可能参与斑块形成和草酸钙肾结石。过去 8 年对各种数据库的检索发现了有关活性氧参与草酸钙肾结石的文献。回顾了文献并讨论了结果。在正常条件下，活性氧的产生受到控制，根据需要增加并调节结晶调节剂的产生。活性氧过度产生或抗氧化剂减少会导致氧化应激、炎症和损伤，并与结石合并症有关。所有主要的慢性炎症标志物都可以在结石患者的尿液中检测到。患者 IαI 和凝血酶蛋白家族的尿排泄量也增加。 NHANES III（国家健康和营养检查调查）最近对 17,695 名参与者进行的一项研究结果显示，有肾结石病史的人的抗氧化剂、胡萝卜素和 β-隐黄素显着降低。动物模型和组织培养研究表明，高草酸盐、草酸钙和磷酸钙晶体会引发肾细胞活性氧介导的炎症反应。草酸钙晶体诱导肾素上调和血管紧张素 II 生成。非吞噬性 NADPH 氧化酶导致蛋白激酶 C 介导的活性氧产生。P-38 MAPK/JNK 转导途径开启。转录因子和生长因子以及产生的次级介质参与其中。趋化剂和骨桥蛋白的产生增加，巨噬细胞浸润晶体周围的肾间质。吞噬细胞 NADPH 氧化酶可能被激活，产生额外的活性氧。出现局部炎症、细胞外基质和纤维化。结晶调节剂在炎症和组织修复中具有重要作用。根据现有数据，兰德尔斑块的形成与身体许多部位的细胞外基质矿化相似。肾间质胶原蛋白矿化，有助于斑块通过间质生长，直到矿化前沿到达乳头状表面上皮。斑块暴露于盆腔尿液也可能是活性氧引发上皮脱落的结果。
Idiopathic calcium oxalate kidney stones form while attached to Randall plaques, the subepithelial deposits on renal papillary surfaces. Plaque formation and growth mechanisms are poorly understood. Plaque formation elsewhere in the body is triggered by reactive oxygen species and oxidative stress. This review explores possible reactive oxygen species involvement in plaque formation and calcium oxalate nephrolithiasis. A search of various databases for the last 8 years identified literature on reactive oxygen species involvement in calcium oxalate nephrolithiasis. The literature was reviewed and results are discussed. Under normal conditions reactive oxygen species production is controlled, increasing as needed and regulating crystallization modulator production. Reactive oxygen species overproduction or decreased antioxidants lead to oxidative stress, inflammation and injury, and are involved in stone comorbidity. All major chronic inflammation markers are detectable in stone patient urine. Patients also have increased urinary excretion of the IαI and the thrombin protein families. Results of a recent study of 17,695 participants in NHANES III (National Health and Nutrition Examination Survey) showed significantly lower antioxidants, carotene and β-cryptoxanthin in those with a kidney stone history. Animal model and tissue culture studies revealed that high oxalate, calcium oxalate and calcium phosphate crystals provoked renal cell reactive oxygen species mediated inflammatory responses. Calcium oxalate crystals induce renin up-regulation and angiotensin II generation. Nonphagocytic NADPH oxidase leads to reactive oxygen species production mediated by protein kinase C. The P-38 MAPK/JNK transduction pathway is turned on. Transcriptional and growth factors, and generated secondary mediators become involved. Chemoattractant and osteopontin production is increased and macrophages infiltrate the renal interstitium around the crystal. Phagocytic NADPH oxidase is probably activated, producing additional reactive oxygen species. Localized inflammation, extracellular matrix and fibrosis develop. Crystallization modulators have a significant role in inflammation and tissue repair. Based on available data, Randall plaque formation is similar to extracellular matrix mineralization at many body sites. Renal interstitial collagen becomes mineralized, assisting plaque growth through the interstitium until the mineralizing front reaches papillary surface epithelium. Plaque exposure to pelvic urine may also be a result of reactive oxygen species triggered epithelial sloughing.
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影响因子：
--
作者：
Boonla, Chanchai;Wunsuwan, Rattiporn;Tosukhowong, Piyaratana
通讯作者：
Tosukhowong, Piyaratana
影响因子：
--
作者：
Khan, SR
通讯作者：
Khan, SR
影响因子：
3
作者：
Evan, Andrew P.
通讯作者：
Evan, Andrew P.
影响因子：
7.4
作者：
Meimaridou, E;Jacobson, J;Hothersall, JS
通讯作者：
Hothersall, JS
DOI：
10.1016/j.juro.2011.10.125
发表时间：
2012-03
期刊：
The Journal of urology
影响因子：
--
作者：
Khan SR;Rodriguez DE;Gower LB;Monga M
通讯作者：
Monga M