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dc.creatorMa, Shuai
dc.creatorSun, Shuhui
dc.creatorLi, Jiaming
dc.creatorFan, Yanling
dc.creatorQu, Jing
dc.creatorSun, Liang
dc.creatorWang, Si
dc.creatorZhang, Yiyuan
dc.creatorYang, Shanshan
dc.creatorLiu, Zunpeng
dc.creatorWu, Zeming
dc.creatorZhang, Sheng
dc.creatorWang, Qiaoran
dc.creatorZheng, Aihua
dc.creatorDuo, Shuguang
dc.creatorYu, Yang
dc.creatorIzpisua Belmonte, Juan Carlos
dc.creatorChan, Piu
dc.creatorZhou, Qi
dc.creatorSong, Moshi
dc.creatorZhang, Weiqi
dc.creatorLiu, Guang-Hui
dc.date.accessioned2020-09-18T16:28:52Z
dc.date.available2020-09-18T16:28:52Z
dc.date.created2020-06-29
dc.identifier.issn1748-7838spa
dc.identifier.otherhttps://www.nature.com/articles/s41422-020-00412-6spa
dc.identifier.urihttp://hdl.handle.net/20.500.12010/13458
dc.format.extent18 páginasspa
dc.format.mimetypeapplication/pdfspa
dc.language.isoengspa
dc.publisherCell Researchspa
dc.sourcereponame:Expeditio Repositorio Institucional UJTLspa
dc.sourceinstname:Universidad de Bogotá Jorge Tadeo Lozanospa
dc.subjectSingle-cell transcriptomic atlasspa
dc.subjectprimate cardiopulmonary agingspa
dc.subjectcardiopulmonaryspa
dc.titleSingle-cell transcriptomic atlas of primate cardiopulmonary agingspa
dc.type.localArtículospa
dc.subject.lembSíndrome respiratorio agudo gravespa
dc.subject.lembCOVID-19spa
dc.subject.lembSARS-CoV-2spa
dc.subject.lembCoronavirusspa
dc.rights.accessrightsinfo:eu-repo/semantics/restrictedAccessspa
dc.type.hasversioninfo:eu-repo/semantics/acceptedVersionspa
dc.rights.localAcceso restringidospa
dc.identifier.doihttps://doi.org/10.1038/s41422-020-00412-6spa
dc.description.abstractenglishAging is a major risk factor for many diseases, especially in highly prevalent cardiopulmonary comorbidities and infectious diseases including Coronavirus Disease 2019 (COVID-19). Resolving cellular and molecular mechanisms associated with aging in higher mammals is therefore urgently needed. Here, we created young and old non-human primate single-nucleus/cell transcriptomic atlases of lung, heart and artery, the top tissues targeted by SARS-CoV-2. Analysis of cell type-specific aging-associated transcriptional changes revealed increased systemic inflammation and compromised virus defense as a hallmark of cardiopulmonary aging. With age, expression of the SARS-CoV-2 receptor angiotensin-converting enzyme 2 (ACE2) was increased in the pulmonary alveolar epithelial barrier, cardiomyocytes, and vascular endothelial cells. We found that interleukin 7 (IL7) accumulated in aged cardiopulmonary tissues and induced ACE2 expression in human vascular endothelial cells in an NF-κB-dependent manner. Furthermore, treatment with vitamin C blocked IL7-induced ACE2 expression. Altogether, our findings depict the first transcriptomic atlas of the aged primate cardiopulmonary system and provide vital insights into age-linked susceptibility to SARS-CoV-2, suggesting that geroprotective strategies may reduce COVID-19 severity in the elderly.spa
dc.type.coarhttp://purl.org/coar/resource_type/c_6501spa


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