tetano
Editor, Senior Moderator
Nat Cell Biol
. 2021 Dec 7.
doi: 10.1038/s41556-021-00796-6. Online ahead of print.
A single-cell transcriptomic landscape of the lungs of patients with COVID-19
Si Wang[SUP] #[/SUP][SUP] 1 2 [/SUP], Xiaohong Yao[SUP] #[/SUP][SUP] 3 4 [/SUP], Shuai Ma[SUP] #[/SUP][SUP] 1 5 [/SUP], Yifang Ping[SUP] #[/SUP][SUP] 3 4 [/SUP], Yanling Fan[SUP] #[/SUP][SUP] 6 [/SUP], Shuhui Sun[SUP] #[/SUP][SUP] 1 [/SUP], Zhicheng He[SUP] #[/SUP][SUP] 3 4 [/SUP], Yu Shi[SUP] #[/SUP][SUP] 3 4 [/SUP], Liang Sun[SUP] #[/SUP][SUP] 7 8 9 [/SUP], Shiqi Xiao[SUP] #[/SUP][SUP] 3 4 [/SUP], Moshi Song[SUP] #[/SUP][SUP] 1 5 10 [/SUP], Jun Cai[SUP] 11 [/SUP], Jiaming Li[SUP] 6 10 [/SUP], Rui Tang[SUP] 3 4 [/SUP], Liyun Zhao[SUP] 2 [/SUP], Chaofu Wang[SUP] 12 [/SUP], Qiaoran Wang[SUP] 6 10 [/SUP], Lei Zhao[SUP] 11 [/SUP], Huifang Hu[SUP] 10 13 [/SUP], Xindong Liu[SUP] 3 4 [/SUP], Guoqiang Sun[SUP] 10 13 [/SUP], Lu Chen[SUP] 3 4 [/SUP], Guoqing Pan[SUP] 8 [/SUP], Huaiyong Chen[SUP] 14 [/SUP], Qingrui Li[SUP] 3 4 [/SUP], Peipei Zhang[SUP] 12 15 [/SUP], Yuanyuan Xu[SUP] 3 4 [/SUP], Huyi Feng[SUP] 16 [/SUP], Guo-Guang Zhao[SUP] 2 17 [/SUP], Tianzi Wen[SUP] 3 4 [/SUP], Yungui Yang[SUP] 5 6 10 [/SUP], Xuequan Huang[SUP] 18 [/SUP], Wei Li[SUP] 5 10 13 [/SUP], Zhenhua Liu[SUP] 19 [/SUP], Hongmei Wang[SUP] 5 10 13 [/SUP], Haibo Wu[SUP] 15 [/SUP], Baoyang Hu[SUP] 5 10 13 [/SUP], Yong Ren[SUP] 20 [/SUP], Qi Zhou[SUP] 5 10 13 [/SUP], Jing Qu[SUP] 21 22 23 [/SUP], Weiqi Zhang[SUP] 24 25 26 27 [/SUP], Guang-Hui Liu[SUP] 28 29 30 31 [/SUP], Xiu-Wu Bian[SUP] 32 33 [/SUP]
Affiliations
Abstract
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.
. 2021 Dec 7.
doi: 10.1038/s41556-021-00796-6. Online ahead of print.
A single-cell transcriptomic landscape of the lungs of patients with COVID-19
Si Wang[SUP] #[/SUP][SUP] 1 2 [/SUP], Xiaohong Yao[SUP] #[/SUP][SUP] 3 4 [/SUP], Shuai Ma[SUP] #[/SUP][SUP] 1 5 [/SUP], Yifang Ping[SUP] #[/SUP][SUP] 3 4 [/SUP], Yanling Fan[SUP] #[/SUP][SUP] 6 [/SUP], Shuhui Sun[SUP] #[/SUP][SUP] 1 [/SUP], Zhicheng He[SUP] #[/SUP][SUP] 3 4 [/SUP], Yu Shi[SUP] #[/SUP][SUP] 3 4 [/SUP], Liang Sun[SUP] #[/SUP][SUP] 7 8 9 [/SUP], Shiqi Xiao[SUP] #[/SUP][SUP] 3 4 [/SUP], Moshi Song[SUP] #[/SUP][SUP] 1 5 10 [/SUP], Jun Cai[SUP] 11 [/SUP], Jiaming Li[SUP] 6 10 [/SUP], Rui Tang[SUP] 3 4 [/SUP], Liyun Zhao[SUP] 2 [/SUP], Chaofu Wang[SUP] 12 [/SUP], Qiaoran Wang[SUP] 6 10 [/SUP], Lei Zhao[SUP] 11 [/SUP], Huifang Hu[SUP] 10 13 [/SUP], Xindong Liu[SUP] 3 4 [/SUP], Guoqiang Sun[SUP] 10 13 [/SUP], Lu Chen[SUP] 3 4 [/SUP], Guoqing Pan[SUP] 8 [/SUP], Huaiyong Chen[SUP] 14 [/SUP], Qingrui Li[SUP] 3 4 [/SUP], Peipei Zhang[SUP] 12 15 [/SUP], Yuanyuan Xu[SUP] 3 4 [/SUP], Huyi Feng[SUP] 16 [/SUP], Guo-Guang Zhao[SUP] 2 17 [/SUP], Tianzi Wen[SUP] 3 4 [/SUP], Yungui Yang[SUP] 5 6 10 [/SUP], Xuequan Huang[SUP] 18 [/SUP], Wei Li[SUP] 5 10 13 [/SUP], Zhenhua Liu[SUP] 19 [/SUP], Hongmei Wang[SUP] 5 10 13 [/SUP], Haibo Wu[SUP] 15 [/SUP], Baoyang Hu[SUP] 5 10 13 [/SUP], Yong Ren[SUP] 20 [/SUP], Qi Zhou[SUP] 5 10 13 [/SUP], Jing Qu[SUP] 21 22 23 [/SUP], Weiqi Zhang[SUP] 24 25 26 27 [/SUP], Guang-Hui Liu[SUP] 28 29 30 31 [/SUP], Xiu-Wu Bian[SUP] 32 33 [/SUP]
Affiliations
- PMID: 34876692
- DOI: 10.1038/s41556-021-00796-6
Abstract
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.