ArticleDevelopmental cell2020
Cigarette Smoke Exposure and Inflammatory Signaling Increase the Expression of the SARS-CoV-2 Receptor ACE2 in the Respiratory Tract.
Article in Developmental cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 260 papers, 7 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
260 citing papers in PubMed, 7 syntheses or guidelines pooled it, 416 citations in OpenAlex.
- Association of the ACE2-Angiotensin1-7-Mas axis with lung damage caused by cigarette smoke exposure: a systematic review.Reviews on environmental health · 2024Pooled it
- Particulate matter air pollution and COVID-19 infection, severity, and mortality: A systematic review and meta-analysis.The Science of the total environment · 2023Pooled it
- Angiotensin converting enzyme 2 level and its significance in COVID-19 and other diseases patients.European journal of clinical investigation · 2023Pooled it
- Factors associated with mortality in patients with COVID-19 admitted to intensive care: a systematic review and meta-analysis.Anaesthesia · 2021Pooled it
- Single-cell meta-analysis of SARS-CoV-2 entry genes across tissues and demographics.Nature medicine · 2021Pooled it
- The effect of smoking on COVID-19 severity: A systematic review and meta-analysis.Journal of medical virology · 2021Pooled it
- Pooled it
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- Unraveling the Enigma of COVID-19 pneumonia and lung diameters: An HR-CT based study.Pakistan journal of medical sciences · 2026Article
- Human keratinocytes exhibit limited potential for SARS-CoV-2 infection despite ACE2 and mature cathepsin L expression.JID innovations : skin science from molecules to population health · 2026Article
- The Role of Immunosenescence and Inflammaging in the Susceptibility of Older Adults to SARS-CoV-2 Infection.Current pharmaceutical biotechnology · 2026Review
- Biological Plausibility Between Long-COVID and Periodontal Disease Development or Progression.Biomedicines · 2025Review
- Circulating Cardiovascular Proteomic Associations With Genetics and Disease.Circulation. Genomic and precision medicine · 2025Article
- Article
- ACE-2 blockade and TMPRSS2 inhibition mitigate SARS-CoV-2 severity following cigarette smoke exposure in airway epithelial cellsMolecular therapy. Nucleic acids · 2025Article
- Increased Cerebrospinal Fluid Angiotensin-Converting Enzyme 2 Fragments as a Read-Out of Brain Infection in Patients With COVID-19 Encephalopathy.The Journal of infectious diseases · 2025Article
- Dynamic Interaction Between SARS-CoV-2 and Influenza A Virus Infection in Human Respiratory Tissues and Cells.Microorganisms · 2025Article
- Mathematical modelling of the heterogeneity of disease progression and treatment outcomes in patients with COVID-19.Frontiers in microbiology · 2025Article
- Association between long-term smoking cessation and COVID-19 outcomes: Findings from a nationwide crosssectional online survey in China.Tobacco induced diseases · 2025Article
200 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The factors mediating fatal SARS-CoV-2 infections are poorly understood. Here, we show that cigarette smoke causes a dose-dependent upregulation of angiotensin converting enzyme 2 (ACE2), the SARS-CoV-2 receptor, in rodent and human lungs. Using single-cell sequencing data, we demonstrate that ACE2 is expressed in a subset of secretory cells in the respiratory tract. Chronic smoke exposure triggers the expansion of this cell population and a concomitant increase in ACE2 expression. In contrast, quitting smoking decreases the abundance of these secretory cells and reduces ACE2 levels. Finally, we demonstrate that ACE2 expression is responsive to inflammatory signaling and can be upregulated by viral infections or interferon treatment. Taken together, these results may partially explain why smokers are particularly susceptible to severe SARS-CoV-2 infections. Furthermore, our work identifies ACE2 as an interferon-stimulated gene in lung cells, suggesting that SARS-CoV-2 infections could create positive feedback loops that increase ACE2 levels and facilitate viral dissemination.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.