Institute of Cellular and System Medicine, National Health Research Institutes, Zhunan, Taiwan.
Toxicol Mech Methods. 2012 Jun;22(5):323-9. doi: 10.3109/15376516.2012.666685. Epub 2012 Mar 21.
In the US, lung disease is the number three killer and accounts for one of every six deaths. Furthermore, more than 35 million US populations are now living with a chronic lung disease. Therefore, it is of urgent need to develop novel strategies that can protect against the development and progression of lung disease. Inhalation of air pollutants or environmental toxins induces inflammation and oxidative stress in the lung, resulting in tissue damage with subsequent decline in lung function. Heme oxygenase-1 (HO-1) is a stress response protein, which is highly inducible in response to pathological stimulation. Due to the cumulative effects of HO-1 on heme catabolism and the generation of biologically active downstream products, induction of HO-1 might serve as a protective mechanism against oxidative stress and inflammation-induced injury. Accumulating evidences have indicated a protective function of HO-1 against lung injury. This review highlights the roles of HO-1 in lung disease induced by environmental toxins such as cigarette smoke (CS), silica, and asbestos.
在美国,肺部疾病是第三大致死原因,占死亡人数的六分之一。此外,目前有超过 3500 万的美国人口患有慢性肺部疾病。因此,迫切需要开发新的策略来预防肺部疾病的发展和恶化。空气污染物或环境毒素的吸入会在肺部引起炎症和氧化应激,导致组织损伤,随后肺功能下降。血红素加氧酶-1(HO-1)是一种应激反应蛋白,对病理刺激有高度诱导作用。由于 HO-1 对血红素分解代谢和生物活性下游产物生成的累积效应,HO-1 的诱导可能是对抗氧化应激和炎症诱导损伤的一种保护机制。越来越多的证据表明 HO-1 对肺部损伤具有保护作用。本综述强调了 HO-1 在环境毒素(如香烟烟雾(CS)、二氧化硅和石棉)引起的肺部疾病中的作用。