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  • A single-cell transcriptomic landscape of the lungs of patients with COVID-19 #MMPMID34876692
  • Wang S; Yao X; Ma S; Ping Y; Fan Y; Sun S; He Z; Shi Y; Sun L; Xiao S; Song M; Cai J; Li J; Tang R; Zhao L; Wang C; Wang Q; Zhao L; Hu H; Liu X; Sun G; Chen L; Pan G; Chen H; Li Q; Zhang P; Xu Y; Feng H; Zhao GG; Wen T; Yang Y; Huang X; Li W; Liu Z; Wang H; Wu H; Hu B; Ren Y; Zhou Q; Qu J; Zhang W; Liu GH; Bian XW
  • Nat Cell Biol 2021[Dec]; 23 (12): 1314-1328 PMID34876692show ga
  • The lung is the primary organ targeted by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), making respiratory failure a leading coronavirus disease 2019 (COVID-19)-related mortality. However, our cellular and molecular understanding of how SARS-CoV-2 infection drives lung pathology is limited. Here we constructed multi-omics and single-nucleus transcriptomic atlases of the lungs of patients with COVID-19, which integrate histological, transcriptomic and proteomic analyses. Our work reveals the molecular basis of pathological hallmarks associated with SARS-CoV-2 infection in different lung and infiltrating immune cell populations. We report molecular fingerprints of hyperinflammation, alveolar epithelial cell exhaustion, vascular changes and fibrosis, and identify parenchymal lung senescence as a molecular state of COVID-19 pathology. Moreover, our data suggest that FOXO3A suppression is a potential mechanism underlying the fibroblast-to-myofibroblast transition associated with COVID-19 pulmonary fibrosis. Our work depicts a comprehensive cellular and molecular atlas of the lungs of patients with COVID-19 and provides insights into SARS-CoV-2-related pulmonary injury, facilitating the identification of biomarkers and development of symptomatic treatments.
  • |Alveolar Epithelial Cells/metabolism/pathology/virology[MESH]
  • |COVID-19/*genetics/metabolism[MESH]
  • |Fibrosis/metabolism/pathology/virology[MESH]
  • |Humans[MESH]
  • |Lung/*metabolism/pathology/virology[MESH]
  • |Proteomics/methods[MESH]
  • |SARS-CoV-2/pathogenicity[MESH]
  • |Transcriptome/*genetics[MESH]

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  • suck abstract from ncbi

    1314 12.23 2021