Oxidative stress in pulmonary fibrosis - A possible role for redox modulatory therapy
Oxidative stress in pulmonary fibrosis - A possible role for redox modulatory therapy
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DOI：
10.1164/rccm.200501-017pp
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发表时间：
2005-08-15
影响因子：
24.7
通讯作者：
Oury, TD
中科院分区：
文献类型：
--
作者：
Kinnula, VL;Fattman, CL;Oury, TD
特发性肺纤维化（普通型间质性肺炎的组织病理学）是一种病因不明的进行性肺部疾病。没有治疗显示出改善患有这种疾病的患者的预后。最近的证据，包括观察到特发性肺纤维化患者的氧化应激水平高于对照组患者，以及最近欧洲多中心研究检查抗氧化剂N-乙酰半胱氨酸对特发性肺纤维化进展的影响，表明细胞氧化还原状态可能在这种疾病的进展中发挥重要作用。这些复杂的机制包括生长因子的激活以及基质金属蛋白酶和蛋白酶抑制剂的调节。未来治疗间质性肺纤维化的潜在方法可能涉及能够调节细胞氧化还原状态的合成药物。研究抑制氧化剂介导的反应在肺纤维化的发生和发展中的治疗方法可能为这种疾病的未来治疗提供希望。
Idiopathic ulmonary fibrosis (histopathology of usual interstitial pneumonia) is a progressive lung disease of unknown etiology. No treatment has been shown to improve the prognosis of the patients with this disease. Recent evidence, including the observations that the patients with idiopathic pulmonary fibrosis have higher levels of oxidant stress than control patients, and a recent multicenter European study examining the effect of the antioxidant N-acetylcysteine on the progression of idiopathic pulmonary fibrosis suggest that the cellular redox state may play a significant roles in the progression of this disease. These complex mechanisms include activation of growth factors as well as regulation of matrix metalloproteinases and protease inhibitors. Potential future approaches for the therapy of interstitial pulmonary fibrosis may involve synthetic agents able to modulate cellular redox state. Investigation into therapeutic approaches to inhibit oxidant-mediated reactions in the initiation and progression of pulmonary fibrosis may provide hope for the future treatment of this disease.