School of Life Sciences, BS Abdur Rahman Crescent Institute of Science & Technology, Chennai, India.
SSE, Saveetha Institute of Medical and Technical Sciences, Chennai, India.
Curr Pharm Des. 2020;26(4):485-491. doi: 10.2174/1381612826666200107144810.
Mitochondria are the crucial regulators for the major source of ATP for different cellular events. Due to damage episodes, mitochondria have been established for a plethora ofalarming signals of stress that lead to cellular deterioration, thereby causing programmed cell death. Defects in mitochondria play a key role in arbitrating pathophysiological machinery with recent evince delineating a constructive role in mitophagy mediated mitochondrial injury. Mitophagy has been known for the eradication of damaged mitochondria via the autophagy process. Mitophagy has been investigated as an evolutionarily conserved mechanism for mitochondrial quality control and homeostasis. Impaired mitophagy has been critically linked with the pathogenesis of inflammatory diseases. Nevertheless, the exact mechanism is not quite revealed, and it is still debatable. The purpose of this review was to investigate the possible role of mitophagy and its associated mechanism in inflammation-mediated diseases at both the cellular and molecular levels.
线粒体是不同细胞事件中 ATP 主要来源的关键调节者。由于损伤事件的发生，线粒体已经产生了大量的应激警报信号，这些信号会导致细胞恶化，从而引发程序性细胞死亡。线粒体缺陷在调解生理病理机制中起着关键作用，最近的证据表明，在线粒体损伤介导的自噬中发挥着建设性的作用。自噬过程通过自噬作用来清除受损的线粒体，这一点已经为人所知。自噬被认为是一种进化上保守的机制，用于维持线粒体的质量控制和动态平衡。受损的自噬与炎症性疾病的发病机制密切相关。然而，确切的机制尚未完全揭示，这仍然存在争议。本综述的目的是探讨自噬及其相关机制在细胞和分子水平上炎症介导的疾病中的可能作用。
