ArticleBMC research notes2025
Peripheral alveolar macrophages express more ACE2 immunoreactivity than in hilar area in human autopsied lung.
Article in BMC research notes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Efferocytosis of apoptotic bodies drives SARS-CoV-2 infection and macrophage inflammation.Nature communications · 2026Article
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Authors and funding
6 authors.
Funding
Abstract
objectiveSARS-coronavirus 2 (SARS-CoV-2) is the cause of the coronavirus disease 19 (COVID-19). SARS-CoV-2 spike (S) glycoprotein binds to a cellular receptor angiotensin converting enzyme 2 (ACE2). COVID-19 pneumonia has a tendency to cause peripheral inflammation. To test the possibility that peripheral predominance of COVID-19 pneumonia is dependent on the peripheral expressions of ACE2, ACE2-positive macrophages and type 2 alveolar epithelial cells were immunohistochemically counted under the microscope, and compared between peripheral and hilar lung areas.
resultsOur result shows that peripheral alveolar macrophages express statistically significantly higher positivity in ACE2 than hilar alveolar macrophages. On the other hand, no statistically significant difference is shown in the expression of ACE2 in type 2 alveolar epithelia between peripheral and hilar alveoli. The higher expression of ACE2 immunoreactivity in peripheral alveolar macrophages may contribute to understanding the peripheral susceptibility of COVID-19 pneumonia.
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