首页> 外文期刊>Molecular medicine. >Phosphorylation of Extracellular Signal-Regulated Kinase (ERK)-1/2 Is Associated with the Downregulation of Peroxisome Proliferator–Activated Receptor (PPAR)-γ during Polymicrobial Sepsis
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Phosphorylation of Extracellular Signal-Regulated Kinase (ERK)-1/2 Is Associated with the Downregulation of Peroxisome Proliferator–Activated Receptor (PPAR)-γ during Polymicrobial Sepsis

机译:细胞外信号调节激酶(ERK)-1/2的磷酸化与细菌败血症过程中过氧化物酶体增殖物激活受体(PPAR)-γ的下调有关。

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Sepsis, an overwhelming inflammatory response to infection or injury, may lead to shock, multiple organ failure and death. Peroxisome proliferator-activated receptor-γ (PPARγ) is a transcription factor which regulates inflammation. Post-translational modifications to PPARγ regulate its function, potentially affecting inflammation. In this work, Kaplan et al. investigated the kinetics of altered PPARγ expression and activation in a model of polymicrobial sepsis. Data demonstrate PPARγ is reduced in immunomodulatory and parenchymal cells during polymicrobial sepsis. Restoration of PPARγ correlates with an increase in levels of the antiinflammatory adipokine, adiponectin. These results provide a mechanism through which a decrease in PPARγ in sepsis may be partially explained and support the notion that additional studies investigating the molecular link between adipokines and the inflammatory response in sepsis are warranted.
机译:败血症是对感染或伤害的压倒性炎症反应,可能导致休克,多器官功能衰竭和死亡。过氧化物酶体增殖物激活受体-γ(PPARγ)是调节炎症的转录因子。 PPARγ的翻译后修饰可调节其功能,从而可能影响炎症。在这项工作中,Kaplan等人。研究了多菌败血症模型中PPARγ表达和激活改变的动力学。数据表明,在微生物败血症期间,免疫调节细胞和实质细胞中的PPARγ降低。 PPARγ的恢复与抗炎脂肪因子脂联素水平的增加有关。这些结果提供了一种机制,可以部分解释败血症中PPARγ的降低,并支持这样的观点,即有必要进行更多研究来研究败血症中脂肪因子和炎症反应之间的分子联系。

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