Experimental sepsis-induced mitochondrial biogenesis is dependent on autophagy, TLR4, and TLR9 signaling in liver
Experimental sepsis-induced mitochondrial biogenesis is dependent on autophagy, TLR4, and TLR9 signaling in liver
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DOI：
10.1096/fj.13-229476
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发表时间：
2013-12-01
期刊：
影响因子：
4.8
通讯作者：
Zuckerbraun, Brian S.
中科院分区：
文献类型：
--
作者：
Carchman, Evie H.;Whelan, Sean;Zuckerbraun, Brian S.
脓毒症中的器官损伤最初的特征是功能障碍，没有细胞死亡和结构损伤，因此具有恢复器官功能的能力。脓毒症的适应性代谢反应可以预防生物能量衰竭和死亡。这些研究旨在研究脓毒症对线粒体稳态的影响，重点是去除功能失调的线粒体和恢复健康的线粒体群体。这些数据表明，小鼠盲肠结扎和穿孔（CLP）后8 h肝氧化磷酸化降低31 +/- 11%，LPS处理后12 h肝氧化磷酸化降低34 +/- 9%（P
Organ injury in sepsis is initially characterized by dysfunction without cell death and structural damage, and thus with the ability to recover organ function. Adaptive metabolic responses to sepsis can prevent bioenergetic failure and death. These studies were aimed at investigating the influence of sepsis on mitochondrial homeostasis, focusing on removal of dysfunctional mitochondria and restitution of a healthy mitochondrial population. These data demonstrate decreased hepatic oxidative phosphorylation by 31 +/- 11% following murine cecal ligation and puncture (CLP) at 8 h and 34 +/- 9% following LPS treatment in vitro at 12 h (P