Mohanty Abhishek, Tiwari-Pandey Rashmi, Pandey Nihar R
MVR Cancer Center and Research Institute, Calicut, Kerala, Pin-673601, India.
CliniCan Health Research, Surrey, BC, V3T 0B1, Canada.
J Cell Commun Signal. 2019 Sep;13(3):303-318. doi: 10.1007/s12079-019-00507-9. Epub 2019 Feb 4.
Mitochondria, the dynamic organelles and power house of eukaryotic cells function as metabolic hubs of cells undergoing continuous cycles of fusion and fission. Recent findings have made it increasingly apparent that mitochondria essentially involved in energy production have evolved as principal intracellular signaling platforms regulating not only innate immunity but also inflammatory responses. Perturbations in mitochondrial dynamics, including fusion/fission, electron transport chain (ETC) architecture and cristae organization have now been actively correlated to modulate metabolic activity and immune function of innate and adaptive immune cells. Several newly identified mitochondrial proteins in mitochondrial outer membrane such as mitochondrial antiviral signaling protein (MAVS) and with mitochondrial DNA acting as danger-associated molecular pattern (DAMP) and mitochondrial ROS generated from mitochondrial sources have potentially established mitochondria as key signaling platforms in antiviral immunity in vertebrates and thereby orchestrating adaptive immune cell activations respectively. A thorough understanding of emerging and intervening role of mitochondria in toll-like receptor-mediated innate immune responses and NLRP3 inflammasome complex activation has gained lucidity in recent years that advocates the imposing functions of mitochondria in innate immunity. Fascinatingly, also how the signals stemming from the endoplasmic reticulum co-operate with the mitochondria to activate the NLRP3 inflammasome is now looked ahead as a stage to unravel as to how different mitochondrial and associated organelle stress responses co-operate to bring about inflammatory consequences. This has also opened avenues of research for revealing mitochondrial targets that could be exploited for development of novel therapeutics to treat various infectious, inflammatory, and autoimmune disorders. Thus, this review explores our current understanding of intricate interplay between mitochondria and other cellular processes like autophagy in controlling mitochondrial homeostasis and regulation of innate immunity and inflammatory responses.
线粒体是真核细胞中动态变化的细胞器和能量工厂,作为细胞的代谢中心,经历着持续的融合和裂变循环。最近的研究结果越来越明显地表明,线粒体在能量产生中起着重要作用,它已演变成主要的细胞内信号平台,不仅调节先天免疫,还调节炎症反应。线粒体动力学的扰动,包括融合/裂变、电子传递链(ETC)结构和嵴的组织,现在已被积极地关联到调节先天免疫和适应性免疫细胞的代谢活性和免疫功能。线粒体外膜中几种新发现的线粒体蛋白,如线粒体抗病毒信号蛋白(MAVS),以及线粒体DNA作为危险相关分子模式(DAMP)和线粒体来源产生的线粒体ROS,可能已将线粒体确立为脊椎动物抗病毒免疫中的关键信号平台,从而分别协调适应性免疫细胞的激活。近年来,对线粒体在Toll样受体介导的先天免疫反应和NLRP3炎性小体复合物激活中新兴和干预作用的深入理解已经明晰,这支持了线粒体在先天免疫中的重要功能。有趣的是,内质网产生的信号如何与线粒体协同激活NLRP3炎性小体,现在也被视为一个有待揭示的阶段,即不同的线粒体和相关细胞器应激反应如何协同导致炎症后果。这也为揭示线粒体靶点开辟了研究途径,这些靶点可用于开发治疗各种感染性、炎症性和自身免疫性疾病的新型疗法。因此,本综述探讨了我们目前对线粒体与其他细胞过程(如自噬)之间复杂相互作用的理解,这些相互作用控制着线粒体稳态以及先天免疫和炎症反应的调节。