Department of Physiology and Biochemical Engineering, Mayo Clinic, Rochester, MN, USA.
Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne, UK.
Trends Biochem Sci. 2019 Dec;44(12):996-1008. doi: 10.1016/j.tibs.2019.06.011. Epub 2019 Jul 22.
Cellular senescence is a major driver of age-related diseases, and senotherapies are being tested in clinical trials. Despite its popularity, cellular senescence is weakly defined and is frequently referred to as irreversible cell-cycle arrest. In this article we hypothesize that cellular senescence is a phenotype that results from the coordination of two processes: cell expansion and cell-cycle arrest. We provide evidence for the compatibility of the proposed model with recent findings showing senescence in postmitotic tissues, wound healing, obesity, and development. We believe our model also explains why some characteristics of senescence can be found in non-senescent cells. Finally, we propose new avenues for research from our model.
细胞衰老（cellular senescence）是与年龄相关疾病的主要驱动因素，衰老疗法正在临床试验中进行测试。尽管细胞衰老（cellular senescence）很受欢迎，但它的定义很弱，通常被称为不可逆的细胞周期停滞。在本文中，我们假设细胞衰老（cellular senescence）是由两个过程协调产生的表型：细胞扩张和细胞周期停滞。我们提供了证据，证明所提出的模型与最近的发现是一致的，这些发现表明细胞衰老（cellular senescence）存在于有丝分裂后组织、伤口愈合、肥胖和发育中。我们相信，我们的模型还解释了为什么一些衰老（senescence）的特征可以在非衰老（senescent）细胞中找到。最后，我们从我们的模型中提出了新的研究途径。
