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10.1038/s41467-020-20323-9

http://scihub22266oqcxt.onion/10.1038/s41467-020-20323-9
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33397975!7782551!33397975
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suck abstract from ncbi


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pmid33397975      Nat+Commun 2021 ; 12 (1): 4
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  • The aging transcriptome and cellular landscape of the human lung in relation to SARS-CoV-2 #MMPMID33397975
  • Chow RD; Majety M; Chen S
  • Nat Commun 2021[Jan]; 12 (1): 4 PMID33397975show ga
  • Age is a major risk factor for severe coronavirus disease-2019 (COVID-19). Here, we interrogate the transcriptional features and cellular landscape of the aging human lung. By intersecting these age-associated changes with experimental data on SARS-CoV-2, we identify several factors that may contribute to the heightened severity of COVID-19 in older populations. The aging lung is transcriptionally characterized by increased cell adhesion and stress responses, with reduced mitochondria and cellular replication. Deconvolution analysis reveals that the proportions of alveolar type 2 cells, proliferating basal cells, goblet cells, and proliferating natural killer/T cells decrease with age, whereas alveolar fibroblasts, pericytes, airway smooth muscle cells, endothelial cells and IGSF21(+) dendritic cells increase with age. Several age-associated genes directly interact with the SARS-CoV-2 proteome. Age-associated genes are also dysregulated by SARS-CoV-2 infection in vitro and in patients with severe COVID-19. These analyses illuminate avenues for further studies on the relationship between age and COVID-19.
  • |A549 Cells[MESH]
  • |Adult[MESH]
  • |Aged[MESH]
  • |Aging/*genetics/metabolism/pathology[MESH]
  • |COVID-19/*genetics/metabolism/pathology/virology[MESH]
  • |Endothelial Cells/pathology[MESH]
  • |Female[MESH]
  • |Fibroblasts/pathology[MESH]
  • |Gene Expression[MESH]
  • |Humans[MESH]
  • |Lung/metabolism/pathology/*physiology/virology[MESH]
  • |Male[MESH]
  • |Middle Aged[MESH]
  • |Pericytes/pathology[MESH]
  • |RNA-Seq[MESH]
  • |SARS-CoV-2/isolation & purification[MESH]
  • |Transcriptome[MESH]


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