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加剧香烟烟雾引起的肺功能障碍。

p19 Exacerbates Cigarette Smoke-Induced Pulmonary Dysfunction.

机构信息

Research Institute, National Center for Geriatrics and Gerontology, Obu, Aichi 474-8511, Japan.

Department of Respiratory Medicine, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.

出版信息

Biomolecules. 2020 Mar 17;10(3):462. doi: 10.3390/biom10030462.

DOI:10.3390/biom10030462
PMID:32192082
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7175375/
Abstract

Senescent cells accumulate in tissues during aging or pathological settings. The semi-genetic or pharmacological targeting of senescent cells revealed that cellular senescence underlies many aspects of the aging-associated phenotype and diseases. We previously reported that cellular senescence contributes to aging- and disease-associated pulmonary dysfunction. We herein report that the elimination of -expressing cells ameliorates cigarette smoke-induced lung pathologies in mice. Cigarette smoke induced the expression of and in lung tissue with concomitant increases in lung tissue compliance and alveolar airspace. The elimination of -expressing cells prior to cigarette smoke exposure protected against these changes. Furthermore, the administration of cigarette smoke extract lead to pulmonary dysfunction, which was ameliorated by subsequent senescent cell elimination. Collectively, these results suggest that senescent cells are a potential therapeutic target for cigarette smoking-associated lung disease.

摘要

衰老细胞在衰老或病理环境中积累在组织中。衰老细胞的半遗传或药理学靶向治疗揭示了细胞衰老是衰老相关表型和疾病的许多方面的基础。我们之前报道过,细胞衰老导致与衰老和疾病相关的肺功能障碍。我们在此报告,表达细胞的消除可改善香烟烟雾引起的小鼠肺部病变。香烟烟雾诱导肺组织中表达和 ,同时肺组织顺应性和肺泡气腔增加。在香烟烟雾暴露之前消除表达细胞可防止这些变化。此外,香烟烟雾提取物的给予导致肺功能障碍,随后消除衰老细胞可改善这种情况。总之,这些结果表明衰老细胞是与吸烟相关的肺部疾病的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0659/7175375/caaaa946ac07/biomolecules-10-00462-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0659/7175375/2cf0334e3a68/biomolecules-10-00462-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0659/7175375/2960875d53ac/biomolecules-10-00462-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0659/7175375/23e310bbef3c/biomolecules-10-00462-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0659/7175375/db6fe5078f37/biomolecules-10-00462-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0659/7175375/4263f7c0ebaf/biomolecules-10-00462-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0659/7175375/caaaa946ac07/biomolecules-10-00462-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0659/7175375/2cf0334e3a68/biomolecules-10-00462-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0659/7175375/2960875d53ac/biomolecules-10-00462-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0659/7175375/23e310bbef3c/biomolecules-10-00462-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0659/7175375/db6fe5078f37/biomolecules-10-00462-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0659/7175375/4263f7c0ebaf/biomolecules-10-00462-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0659/7175375/caaaa946ac07/biomolecules-10-00462-g006.jpg

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本文引用的文献

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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。
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Elimination of p19 -expressing cells protects against pulmonary emphysema in mice.消除表达 p19 的细胞可预防小鼠肺气肿。
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Lung cellular senescence is independent of aging in a mouse model of COPD/emphysema.
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Cellular senescence promotes cancer metastasis by enhancing soluble E-cadherin production.细胞衰老通过增强可溶性E-钙黏蛋白的产生促进癌症转移。
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