Cellular Senescence in Aging Lungs and Diseases

被引:37
作者
Aghali, Arbi [1 ]
Ngassie, Maunick Lefin Koloko [2 ,3 ,4 ]
Pabelick, Christina M. [1 ,5 ]
Prakash, Y. S. [1 ,5 ]
机构
[1] Mayo Clin, Dept Physiol & Biomed Engn, Rochester, MN 55905 USA
[2] Univ Groningen, Univ Med Ctr Groningen, Dept Pathol & Med Biol, NL-9713 GZ Groningen, Netherlands
[3] Univ Groningen, Univ Med Ctr Groningen, Groningen Res Inst Asthma, NL-9700 RB Groningen, Netherlands
[4] Univ Groningen, Univ Med Ctr Groningen, COPD, NL-9700 RB Groningen, Netherlands
[5] Mayo Clin, Dept Anesthesiol & Perioperat Med, Rochester, MN 55905 USA
关键词
aging; senescence; lung diseases; asthma; COPD; pulmonary fibrosis; remodeling; mitochondrial dysfunction; NF-KAPPA-B; ACTIVATED PROTEIN-KINASE; IDIOPATHIC PULMONARY-FIBROSIS; MITOCHONDRIAL-DNA DAMAGE; AIRWAY SMOOTH-MUSCLE; INFLAMMATORY RESPONSES; TELOMERE DYSFUNCTION; SECRETORY PHENOTYPE; HYDROGEN-PEROXIDE; OXIDATIVE STRESS;
D O I
10.3390/cells11111781
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
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页数:16
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