Alveolar cell death in hyperoxia-induced lung injury
Alveolar cell death in hyperoxia-induced lung injury
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DOI：
10.1196/annals.1299.074
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发表时间：
2003-01-01
期刊：
影响因子：
--
通讯作者：
Barazzone-Argiroffo, C
中科院分区：
文献类型：
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作者：
Pagano, A;Barazzone-Argiroffo, C
暴露在高氧浓度下，通过增加活性氧物种的产生，导致细胞直接氧化损伤。在体内，氧诱导的肺损伤在啮齿类动物身上有很好的特征，并已被用作人类呼吸窘迫综合征的有价值的模型。高氧性肺损伤可被认为是一个双峰过程，其结果是(1)直接氧中毒和(2)炎症介质在肺内积聚。在高氧状态下，肺泡细胞(主要是上皮细胞和内皮细胞)发生了细胞凋亡和坏死。虽然在组织培养中，体外对氧气的反应似乎依赖于细胞类型，但仍不清楚体内涉及哪些死亡机制和途径。尽管尚不能明确区分细胞凋亡、坏死或其他中间形式的细胞死亡(S)，但已有许多不同的策略被证明可以防止高氧时的肺泡损伤和提高动物的存活率。在这篇综述中，我们总结了高氧时导致肺泡损伤的不同细胞死亡途径，特别是线粒体的关键作用。此外，我们还讨论了可能干扰肺泡细胞死亡的不同保护机制。
Exposure to high oxygen concentration causes direct oxidative cell damage through increased production of reactive oxygen species. In vivo oxygen-induced lung injury is well characterized in rodents and has been used as a valuable model of human respiratory distress syndrome. Hyperoxia-induced lung injury can be considered as a bimodal process resulting (1) from direct oxygen toxicity and (2) from the accumulation of inflammatory mediators within the lungs. Both apoptosis and necrosis have been described in alveolar cells (mainly epithelial and endothelial) during hyperoxia. While the in vitro response to oxygen seems to be cell type-dependent in tissue cultures, it is still unclear which are the death mechanisms and pathways implicated in vivo. Even though it is not yet possible to distinguish unequivocally between apoptosis, necrosis, or other intermediate form(s) of cell death, a great variety of strategies has been shown to prevent alveolar damage and to increase animal survival during hyperoxia. In this review, we summarize the different cell death pathways leading to alveolar damage during hyperoxia, with particular attention to the pivotal role of mitochondria. In addition, we discuss the different protective mechanisms potentially interfering with alveolar cell death.