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本文引用的文献

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Circadian control of lung inflammation in influenza infection.流感感染中肺炎症的昼夜节律控制。
Nat Commun. 2019 Sep 11;10(1):4107. doi: 10.1038/s41467-019-11400-9.
2
The Nuclear Receptor and Clock Repressor Rev-erbα Suppresses Myogenesis.核受体和时钟负调控因子 Rev-erbα 抑制成肌分化。
Sci Rep. 2019 Mar 14;9(1):4585. doi: 10.1038/s41598-019-41059-7.
3
Tissue-specific BMAL1 cistromes reveal that rhythmic transcription is associated with rhythmic enhancer-enhancer interactions.组织特异性 BMAL1 顺式作用元件组揭示了节律性转录与节律性增强子-增强子相互作用有关。
Genes Dev. 2019 Mar 1;33(5-6):294-309. doi: 10.1101/gad.322198.118. Epub 2019 Feb 25.
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Genome-wide effect of pulmonary airway epithelial cell-specific deletion.肺气道上皮细胞特异性缺失的全基因组效应
FASEB J. 2019 May;33(5):6226-6238. doi: 10.1096/fj.201801682R. Epub 2019 Feb 22.
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Intestinal Stem Cells Exhibit Conditional Circadian Clock Function.肠干细胞表现出条件性的生物钟功能。
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BMAL1 suppresses ROS-induced endothelial-to-mesenchymal transition and atherosclerosis plaque progression via BMP signaling.BMAL1通过骨形态发生蛋白(BMP)信号通路抑制活性氧(ROS)诱导的内皮-间充质转化和动脉粥样硬化斑块进展。
Am J Transl Res. 2018 Oct 15;10(10):3150-3161. eCollection 2018.
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Knocking down clock control gene CRY1 decreases adipogenesis via canonical Wnt/β-catenin signaling pathway.敲低生物钟基因 CRY1 通过经典 Wnt/β-连环蛋白信号通路减少脂肪生成。
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Cryptochrome 1 promotes osteogenic differentiation of human osteoblastic cells via Wnt/β-Catenin signaling.CRY1 通过 Wnt/β-Catenin 信号通路促进人成骨细胞的成骨分化。
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Circadian clock protein BMAL1 regulates IL-1β in macrophages via NRF2.生物钟蛋白 BMAL1 通过 NRF2 调节巨噬细胞中的 IL-1β。
Proc Natl Acad Sci U S A. 2018 Sep 4;115(36):E8460-E8468. doi: 10.1073/pnas.1800431115. Epub 2018 Aug 20.
10
Human lung development: recent progress and new challenges.人类肺脏发育:最新进展与新挑战。
Development. 2018 Aug 15;145(16):dev163485. doi: 10.1242/dev.163485.

发育肺中的时钟。

It's about time: clocks in the developing lung.

机构信息

Department of Anesthesiology and Perioperative Medicine and.

Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.

出版信息

J Clin Invest. 2020 Jan 2;130(1):39-50. doi: 10.1172/JCI130143.

DOI:10.1172/JCI130143
PMID:31895049
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6934206/
Abstract

The discovery of peripheral intracellular clocks revealed circadian oscillations of clock genes and their targets in all cell types, including those in the lung, sparking exploration of clocks in lung disease pathophysiology. While the focus has been on the role of these clocks in adult airway diseases, clock biology is also likely to be important in perinatal lung development, where it has received far less attention. Historically, fetal circadian rhythms have been considered irrelevant owing to lack of external light exposure, but more recent insights into peripheral clock biology raise questions of clock emergence, its concordance with tissue-specific structure/function, the interdependence of clock synchrony and functionality in perinatal lung development, and the possibility of lung clocks in priming the fetus for postnatal life. Understanding the perinatal molecular clock may unravel mechanistic targets for chronic airway disease across the lifespan. With current research providing more questions than answers, it is about time to investigate clocks in the developing lung.

摘要

外周细胞内时钟的发现揭示了时钟基因及其靶基因在所有细胞类型中的昼夜节律振荡,包括肺部细胞,这激发了人们对肺部疾病病理生理学中时钟的探索。虽然这些时钟在成人气道疾病中的作用一直是研究重点,但时钟生物学在围产期肺发育中也可能很重要,但目前对其关注较少。从历史上看,由于胎儿缺乏外部光照,胎儿的昼夜节律一直被认为是无关紧要的,但最近对周围时钟生物学的深入了解提出了时钟出现的问题,其与组织特异性结构/功能的一致性,围产期肺发育中时钟同步和功能的相互依赖性,以及胎儿肺部时钟为出生后生活做好准备的可能性。了解围产期分子时钟可能会揭示整个生命周期慢性气道疾病的机制靶点。目前的研究提出的问题多于答案,是时候研究发育中肺部的时钟了。