高氧
信号转导
激酶
细胞生物学
MAPK/ERK通路
p38丝裂原活化蛋白激酶
ASK1
氧化应激
蛋白激酶A
丝裂原活化蛋白激酶3
活性氧
生物
丝裂原活化蛋白激酶
肺
医学
内科学
内分泌学
丝裂原活化蛋白激酶激酶
作者
Andrea Porzionato,Maria Martina Sfriso,Andrea Mazzatenta,Veronica Macchi,Raffaele De,Camillo Di Giulio
标识
DOI:10.1016/j.resp.2014.12.002
摘要
Exposure to supraphysiological concentrations of oxygen is often applied in clinical practice to enhance oxygenation in acute or chronic lung injury. However, hyperoxic exposure is associated with increased reactive oxygen species production, which can be toxic to pulmonary endothelial and alveolar epithelial cells. Oxidative stress activates the pathways of the mitogen-activated protein kinases family: extracellular signal-regulated kinase (ERK1/2), C-Jun-terminal protein kinase (JNK1/2), and p38 kinase. Several studies have suggested that ERK activation in lung cells has a protective effect in response to hyperoxia, through stimulation of DNA repair and antioxidant mechanisms, and prolonged cell survival. Conversely, JNK1/2 and p38 kinase have been most frequently reported to have roles in induction of apoptotic responses. Moreover, exogenous factors, such as ATP, retinoic acid, substance P, thioredoxin, inosine and laminin, can have cytoprotective effects against hyperoxia-induced cell damage, through promotion of ERK activation and/or limiting JNK and p38 involvement.
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