Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN 55905, USA.
Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, 9713 GZ Groningen, The Netherlands.
Cells. 2022 May 29;11(11):1781. doi: 10.3390/cells11111781.
Cellular senescence represents a state of irreversible cell cycle arrest occurring naturally or in response to exogenous stressors. Following the initial arrest, progressive phenotypic changes define conditions of cellular senescence. Understanding molecular mechanisms that drive senescence can help to recognize the importance of such pathways in lung health and disease. There is increasing interest in the role of cellular senescence in conditions such as chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF) in the context of understanding pathophysiology and identification of novel therapies. Herein, we discuss the current knowledge of molecular mechanisms and mitochondrial dysfunction regulating different aspects of cellular senescence-related to chronic lung diseases to develop rational strategies for modulating the senescent cell phenotype in the lung for therapeutic benefit.
细胞衰老代表一种不可逆的细胞周期停滞状态,可自然发生或响应于外源性应激。初始停滞后,进行性表型变化定义了细胞衰老的条件。了解驱动衰老的分子机制有助于认识这些途径在肺健康和疾病中的重要性。人们对细胞衰老在慢性阻塞性肺疾病(COPD)和特发性肺纤维化(IPF)等疾病中的作用越来越感兴趣,这有助于理解病理生理学和确定新的治疗方法。本文讨论了调节与慢性肺疾病相关的细胞衰老的不同方面的分子机制和线粒体功能障碍的最新知识,以制定合理的策略来调节肺中的衰老细胞表型,从而获得治疗益处。