Department of Biochemistry, Chungbuk National University College of Medicine, Cheongju, 28644, South Korea.
World Class Institute, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Ochang-eup, Cheongju, 28116, South Korea.
Ageing Res Rev. 2021 Jul;68:101332. doi: 10.1016/j.arr.2021.101332. Epub 2021 Mar 19.
Cellular senescence occurs in response to diverse stresses (e.g., telomere shortening, DNA damage, oxidative stress, oncogene activation). A growing body of evidence indicates that alterations in multiple components of endocytic pathways contribute to cellular senescence. Clathrin-mediated endocytosis (CME) and caveolae-mediated endocytosis (CavME) represent major types of endocytosis that are implicated in senescence. More recent research has also identified a chromatin modifier and tumor suppressor that contributes to the induction of senescence via altered endocytosis. Here, molecular regulators of aberrant endocytosis-induced senescence are reviewed and discussed in the context of their capacity to serve as senescence-inducing stressors or modifiers.
细胞衰老发生于对多种应激的反应中（例如端粒缩短、DNA 损伤、氧化应激、致癌基因激活）。越来越多的证据表明，内吞途径的多个组成部分的改变会导致细胞衰老。网格蛋白介导的内吞作用（CME）和小窝蛋白介导的内吞作用（CavME）是内吞作用的两种主要形式，与衰老有关。最近的研究还发现了一种染色质修饰因子和肿瘤抑制因子，它通过改变内吞作用促进衰老的发生。在这里，我们综述了异常内吞作用诱导衰老的分子调控因子，并讨论了它们作为诱导衰老的应激因子或修饰因子的能力。
