Upregulation of ACE2 and TMPRSS2 by particulate matter and idiopathic pulmonary fibrosis: a potential role in severe COVID-19.
Hsin-Hsien LiChen-Chi LiuTien-Wei HsuJiun-Han LinJyuan-Wei HsuAnna Fen-Yau LiYi-Chen YehShih-Chieh HungHan-Shui HsuPublished in: Particle and fibre toxicology (2021)
These data suggested that risk of SARS-CoV-2 infection and COVID-19 disease severity increased by air pollution exposure and underlying IPF. It can be mediated through upregulating ACE2 and TMPRSS2 in pulmonary fibroblasts, and prevented by blocking the IL-8/CXCR1/2 pathway.
Keyphrases
- idiopathic pulmonary fibrosis
- particulate matter
- air pollution
- coronavirus disease
- sars cov
- respiratory syndrome coronavirus
- interstitial lung disease
- angiotensin converting enzyme
- lung function
- angiotensin ii
- pulmonary hypertension
- electronic health record
- early onset
- cell proliferation
- signaling pathway
- poor prognosis
- chronic obstructive pulmonary disease
- long non coding rna
- data analysis
- artificial intelligence