从疾病的分子足迹到糖尿病肾病的新治疗干预:一个侦探故事。

Toshio Miyata, Kiyoshi Kurokawa, Charles van Ypersele de Strihou
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引用次数: 5

摘要

体内组织氧化损伤是一个涉及多种因素和途径的复杂现象。为了更好地了解人类疾病的生理病理,蛋白质是氧化产物分析的特别有吸引力的目标。蛋白质修饰是生化过程的足迹。它们还有助于确定药物抗氧化作用的机制,并进一步寻找有效抑制氧化蛋白损伤的新型药物。临床上已经使用的几种药物通过其化学结构特征的不同机制干扰氧化蛋白损伤。本文综述了糖尿病肾病中存在的氧化蛋白修饰及其与肾保护抗高血压药物的相关性。我们假设的方法需要进一步的测试。然而,在蛋白质修饰的生物化学方面获得的见解为开发新型糖尿病肾病肾保护剂开辟了新的途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
From molecular footprints of disease to new therapeutic interventions in diabetic nephropathy: a detective story.

Oxidative tissue damage in vivo is a complex phenomenon involving many factors and pathways. Proteins are particularly attractive targets for oxidative products analysis in order to understand better the physiopathology of human diseases. Protein modifications serve as footprints of biochemical processes. They also help ascertain the mechanism of anti-oxidative action of medical drugs and further search for novel agents that inhibit efficiently oxidative protein damage. Several drugs already used clinically interfere with oxidative protein damage through different mechanisms characteristic of their chemical structure. This review delineates the oxidative protein modifications existing in diabetic nephropathy and their regression in association with renoprotective anti-hypertensive agents. Our hypothetical approach will require further testing. Nevertheless, the insights gained on the biochemistry of protein modifications open new avenues towards the development of new classes of renoprotective agents for diabetic nephropathy.

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