Circadian molecular clock disruption in chronic pulmonary diseases

被引：37

作者：

Giri, Allan ^{[1
]}

Wang, Qixin ^{[2
]}

Rahman, Irfan ^{[2
]}

Sundar, Isaac Kirubakaran ^{[1
]}

机构：

[1] Univ Kansas Med Ctr, Dept Internal Med, Div Pulm, Crit Care & Sleep Med, Kansas City, KS 66160 USA

[2] Univ Rochester Med Ctr, Sch Med & Dent, Dept Environm Med, Rochester, NY USA

来源：

TRENDS IN MOLECULAR MEDICINE | 2022年 / 28卷 / 06期

关键词：

CYSTIC-FIBROSIS; NUCLEAR RECEPTOR; GENE-EXPRESSION; INNATE IMMUNITY; DNA-DAMAGE; ROR-ALPHA; BMAL1; SIRT1; REGULATOR; RHYTHM;

D O I：

10.1016/j.molmed.2022.04.002

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The circadian clock is the biochemical oscillator with a near 24-h period that is responsible for generating the circadian rhythms in peripheral organs including the lung. Mounting evidence suggests that circadian clock disruption during chronic lung diseases plays an essential role in augmented oxidative stress, inflammatory regulated autophagy, and alters pulmonary function. Here, we review circadian clock disruption and discuss candidate clock genes that are altered at the transcriptional or translational level in chronic pulmonary diseases. This review aims to provide the current knowledge and understanding of the circadian molecular clock disruption in chronic pulmonary diseases which will further advance the development of novel clock-based therapeutics in the future.

引用

页码：513 / 527

页数：15

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