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本文引用的文献

1
Senolytics in idiopathic pulmonary fibrosis: Results from a first-in-human, open-label, pilot study.特发性肺纤维化中的衰老细胞清除:首次人体、开放标签、先导研究的结果。
EBioMedicine. 2019 Feb;40:554-563. doi: 10.1016/j.ebiom.2018.12.052. Epub 2019 Jan 5.
2
Impaired immune surveillance accelerates accumulation of senescent cells and aging.免疫监视受损会加速衰老细胞的积累和衰老。
Nat Commun. 2018 Dec 21;9(1):5435. doi: 10.1038/s41467-018-07825-3.
3
Hyperoxia-induced Cellular Senescence in Fetal Airway Smooth Muscle Cells.氧诱导的胎儿气道平滑肌细胞衰老。
Am J Respir Cell Mol Biol. 2019 Jul;61(1):51-60. doi: 10.1165/rcmb.2018-0176OC.
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Senescence of bone marrow-derived mesenchymal stem cells from patients with idiopathic pulmonary fibrosis.特发性肺纤维化患者骨髓间充质干细胞的衰老。
Stem Cell Res Ther. 2018 Sep 26;9(1):257. doi: 10.1186/s13287-018-0970-6.
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Mitochondrial dysfunction contributes to the senescent phenotype of IPF lung fibroblasts.线粒体功能障碍导致 IPF 肺成纤维细胞的衰老表型。
J Cell Mol Med. 2018 Dec;22(12):5847-5861. doi: 10.1111/jcmm.13855. Epub 2018 Sep 26.
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Short telomere syndromes cause a primary T cell immunodeficiency.短端粒综合征导致原发性 T 细胞免疫缺陷。
J Clin Invest. 2018 Dec 3;128(12):5222-5234. doi: 10.1172/JCI120216. Epub 2018 Oct 22.
7
Quercetin Enhances Ligand-induced Apoptosis in Senescent Idiopathic Pulmonary Fibrosis Fibroblasts and Reduces Lung Fibrosis In Vivo.槲皮素增强衰老特发性肺纤维化成纤维细胞中配体诱导的细胞凋亡,并减少体内肺纤维化。
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8
Impaired Cytomegalovirus Immunity in Idiopathic Pulmonary Fibrosis Lung Transplant Recipients with Short Telomeres.特发性肺纤维化肺移植受者短端粒导致巨细胞病毒免疫受损。
Am J Respir Crit Care Med. 2019 Feb 1;199(3):362-376. doi: 10.1164/rccm.201805-0825OC.
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Tools for engineering coordinated system behaviour in synthetic microbial consortia.用于工程化合成微生物群落中协调系统行为的工具。
Nat Commun. 2018 Jul 11;9(1):2677. doi: 10.1038/s41467-018-05046-2.
10
Senolytics improve physical function and increase lifespan in old age.衰老细胞清除疗法可改善老年的身体机能并延长寿命。
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细胞衰老:慢性肺部疾病中的特洛伊木马。

Cellular Senescence: The Trojan Horse in Chronic Lung Diseases.

机构信息

1 Aging Institute.

2 Division of Pulmonary Allergy and Critical Care Medicine, and.

出版信息

Am J Respir Cell Mol Biol. 2019 Jul;61(1):21-30. doi: 10.1165/rcmb.2018-0410TR.

DOI:10.1165/rcmb.2018-0410TR
PMID:30965013
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6604222/
Abstract

Senescence is a cell fate decision characterized by irreversible arrest of proliferation accompanied by a senescence-associated secretory phenotype. Traditionally, cellular senescence has been recognized as a beneficial physiological mechanism during development and wound healing and in tumor suppression. However, in recent years, evidence of negative consequences of cellular senescence has emerged, illuminating its role in several chronic pathologies. In this context, senescent cells persist or accumulate and have detrimental consequences. In this review, we discuss the possibility that in chronic obstructive pulmonary disease, persistent senescence impairs wound healing in the lung caused by secretion of proinflammatory senescence-associated secretory phenotype factors and exhaustion of progenitor cells. In contrast, in idiopathic pulmonary fibrosis, chronic senescence in alveolar epithelial cells exacerbates the accumulation of senescent fibroblasts together with production of extracellular matrix. We review how cellular senescence may contribute to lung disease pathology.

摘要

衰老(senescence)是一种细胞命运决定,其特征是不可逆的增殖停滞,并伴有衰老相关分泌表型(senescence-associated secretory phenotype)。传统上,细胞衰老被认为是发育和伤口愈合以及肿瘤抑制过程中的一种有益的生理机制。然而,近年来,细胞衰老的负面后果的证据已经出现,这阐明了其在几种慢性病理中的作用。在这种情况下,衰老细胞持续存在或积累,并产生有害的后果。在这篇综述中,我们讨论了在慢性阻塞性肺疾病(chronic obstructive pulmonary disease)中,持续的衰老通过分泌促炎的衰老相关分泌表型因子和祖细胞耗竭,损害肺部的伤口愈合的可能性。相比之下,在特发性肺纤维化(idiopathic pulmonary fibrosis)中,肺泡上皮细胞的慢性衰老加剧了衰老成纤维细胞的积累以及细胞外基质的产生。我们回顾了细胞衰老如何导致肺部疾病的病理变化。