4.8 Article

Multi-organ proteomic landscape of COVID-19 autopsies

期刊

CELL
卷 184, 期 3, 页码 775-+

出版社

CELL PRESS
DOI: 10.1016/j.cell.2021.01.004

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资金

  1. National Key RAMP
  2. D Program of China [2020YFE0202200]
  3. National Natural Science Foundation of China [81972492, 21904107, 81672086, 81773022, 82072333]
  4. Zhejiang Provincial Natural Science Foundation for Distinguished Young Scholars [LR19C050001]
  5. Key Special Project of Ministry of Science and Technology, China [2020YFC0845700]
  6. Fundamental Research Funds for the Central Universities [2020kfyXGYJ101]
  7. Hangzhou Agriculture and Society Advancement Program [20190101A04]
  8. Westlake Education Foundation
  9. Tencent Foundation

向作者/读者索取更多资源

This study used proteomic analysis to reveal the molecular mechanisms of multi-organ injuries in COVID-19 patients. The data showed significant upregulation of cathepsin L1 in the lung, instead of ACE2. Systemic hyperinflammation, dysregulation of glucose and fatty acid metabolism were detected in multiple organs.
The molecular pathology of multi-organ injuries in COVID-19 patients remains unclear, preventing effective therapeutics development. Here, we report a proteomic analysis of 144 autopsy samples from seven organs in 19 COVID-19 patients. We quantified 11,394 proteins in these samples, in which 5,336 were perturbed in the COVID-19 patients compared to controls. Our data showed that cathepsin L1, rather than ACE2, was significantly upregulated in the lung from the COVID-19 patients. Systemic hyperinflammation and dysregulation of glucose and fatty acid metabolism were detected in multiple organs. We also observed dysregulation of key factors involved in hypoxia, angiogenesis, blood coagulation, and fibrosis in multiple organs from the COVID-19 patients. Evidence for testicular injuries includes reduced Leydig cells, suppressed cholesterol biosynthesis, and sperm mobility. In summary, this study depicts a multi-organ proteomic landscape of COVID-19 autopsies that furthers our understanding of the biological basis of COVID-19 pathology.

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