Department of Biomedical Sciences, University of Padua, via Ugo Bassi 58/B, Padua, Italy.
Department of Biomedical Sciences, University of Padua, via Ugo Bassi 58/B, Padua, Italy; Neuroscience Institute, National Research Council of Italy (CNR), via Ugo Bassi 58/B, Padua, Italy.
Cell Calcium. 2021 Mar;94:102344. doi: 10.1016/j.ceca.2020.102344. Epub 2021 Jan 2.
Mitochondrial reactive oxygen species (mROS) are routinely produced at several sites within the organelle. The balance in their formation and elimination is maintained by a complex and robust antioxidant system. mROS may act as second messengers and regulate a number of physiological processes, such as insulin signaling, cell differentiation and proliferation, wound healing, etc. Nevertheless, when a sudden or sustained increase in ROS formation is not efficiently neutralized by the endogenous antioxidant defense system, the detrimental impact of high mROS levels on cell function and viability eventually results in disease development. In this review, we will focus on the dual role of mROS in pathophysiology, emphasizing the physiological role exerted by a regulated mROS production/elimination, and discussing the detrimental effects evoked by an imbalance in mitochondrial redox state. Furthermore, we will touch upon the interplay between mROS and Ca homeostasis.
线粒体活性氧（mROS）通常在细胞器内的几个部位产生。其形成和消除的平衡由一个复杂而强大的抗氧化系统维持。mROS 可以作为第二信使，调节许多生理过程，如胰岛素信号转导、细胞分化和增殖、伤口愈合等。然而，当 ROS 形成的突然或持续增加不能被内源性抗氧化防御系统有效中和时，高 mROS 水平对细胞功能和活力的有害影响最终导致疾病的发展。在这篇综述中，我们将重点讨论 mROS 在病理生理学中的双重作用，强调受调控的 mROS 产生/消除所发挥的生理作用，并讨论线粒体氧化还原状态失衡所引起的有害影响。此外，我们还将探讨 mROS 与钙稳态之间的相互作用。
