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The role of mitophagy in pulmonary sepsis
Mitochondrion ( IF 4.4 ) Pub Date : 2021-04-22 , DOI: 10.1016/j.mito.2021.04.009
Mohd Mohsin 1 , Gulnaz Tabassum 1 , Shaniya Ahmad 1 , Shakir Ali 2 , Mansoor Ali Syed 1
Affiliation  

Sepsis is a systemic inflammatory disease with an unacceptably high mortality rate caused by an infection or trauma that involves both innate and adaptive immune systems. Inflammatory events activate different downstream pathways leading to tissue damage and ultimately multi-organ failure. Mitochondria are responsible for cellular energy, thermoregulation, metabolite biosynthesis, intracellular calcium regulation, and cell death. Damaged mitochondria induce the high Ca2+ influx through mitochondrial calcium uniporter (MCU). It also generates excessive Reactive oxygen species (ROS) and releases mtDNA into the cytoplasm, which causes induction of NLRP3 inflammasome and apoptosis. Mitophagy (Autophagy of damaged mitochondria) controls mitochondrial dynamics and function. It also maintains cellular homeostasis. This review is about how pulmonary sepsis affects the body. What is the aftermath of sepsis, and how mitophagy affects Acute Lung Injury and macrophage polarisation to overcome the damages.



中文翻译:

线粒体自噬在肺脓毒症中的作用

脓毒症是一种全身性炎症性疾病,由感染或创伤引起的死亡率高得令人无法接受,这种疾病涉及先天性和适应性免疫系统。炎症事件激活不同的下游通路,导致组织损伤并最终导致多器官衰竭。线粒体负责细胞能量、体温调节、代谢物生物合成、细胞内钙调节和细胞死亡。受损的线粒体诱导高 Ca 2+通过线粒体钙单向转运体 (MCU) 流入。它还会产生过量的活性氧 (ROS) 并将 mtDNA 释放到细胞质中,从而导致 NLRP3 炎性体的诱导和细胞凋亡。线粒体自噬(受损线粒体的自噬)控制线粒体动力学和功能。它还维持细胞稳态。这篇综述是关于肺脓毒症如何影响身体的。脓毒症的后果是什么,线粒体自噬如何影响急性肺损伤和巨噬细胞极化以克服损害。

更新日期:2021-04-30
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