Research Center for Translational Medicine, Sirius University of Science and Technology, 354340 Sochi, Russia.
Institute of Translational Medicine and Biotechnology, Sechenov First Moscow State Medical University, 119991 Moscow, Russia.
Int J Mol Sci. 2024 Apr 6;25(7):4087. doi: 10.3390/ijms25074087.
Cellular survival hinges on a delicate balance between accumulating damages and repair mechanisms. In this intricate equilibrium, oxidants, currently considered physiological molecules, can compromise vital cellular components, ultimately triggering cell death. On the other hand, cells possess countermeasures, such as autophagy, which degrades and recycles damaged molecules and organelles, restoring homeostasis. Lysosomes and their enzymatic arsenal, including cathepsins, play critical roles in this balance, influencing the cell's fate toward either apoptosis and other mechanisms of regulated cell death or autophagy. However, the interplay between reactive oxygen species (ROS) and cathepsins in these life-or-death pathways transcends a simple cause-and-effect relationship. These elements directly and indirectly influence each other's activities, creating a complex web of interactions. This review delves into the inner workings of regulated cell death and autophagy, highlighting the pivotal role of ROS and cathepsins in these pathways and their intricate interplay.
细胞的存活取决于积累的损伤和修复机制之间的微妙平衡。在这个复杂的平衡中，氧化剂，目前被认为是生理分子，可以破坏重要的细胞成分，最终引发细胞死亡。另一方面，细胞有对策，如自噬，它可以降解和回收受损的分子和细胞器，恢复体内平衡。溶酶体及其酶库，包括组织蛋白酶，在这种平衡中起着关键作用，影响细胞的命运是凋亡和其他形式的细胞程序性死亡还是自噬。然而，活性氧（ROS）和组织蛋白酶之间在这些生死途径中的相互作用超出了简单的因果关系。这些因素直接和间接地影响彼此的活性，形成了一个复杂的相互作用网络。这篇综述深入探讨了细胞程序性死亡和自噬的内在机制，强调了 ROS 和组织蛋白酶在这些途径中的关键作用及其复杂的相互作用。
