Evidence map›Paper›PMID 36868468›Full record

ArticleThe American journal of pathology2023

Lung Remodeling Regions in Long-Term Coronavirus Disease 2019 Feature Basal Epithelial Cell Reprogramming.

Kangyun Wu, Yong Zhang, Stephen R Austin, Huiqing Yin-Declue, Derek E Byers, Erika C Crouch, Michael J Holtzman

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
5.7field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. RelA Signaling inInternational journal of molecular sciences · 2026
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  8. The post-viral GPNMBmedRxiv : the preprint server for health sciences · 2024
    Article
  9. Article
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  11. Mitogen-activated protein kinase-guided drug discovery for post-viral and related types of lung disease.European respiratory review : an official journal of the European Respiratory Society · 2024
    Article
  12. A potent MAPK13-14 inhibitor prevents airway inflammation and mucus production.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  13. Article
  14. Article
  15. An alternative mechanism for skeletal muscle dysfunction in long-term post-viral lung disease.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  16. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Kangyun WuPulmonary and Critical Care Medicine, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri.
Yong ZhangPulmonary and Critical Care Medicine, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri.
Stephen R AustinPulmonary and Critical Care Medicine, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri.
Huiqing Yin-DecluePulmonary and Critical Care Medicine, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri.
Derek E ByersPulmonary and Critical Care Medicine, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri.
Erika C CrouchDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri.
Michael J HoltzmanPulmonary and Critical Care Medicine, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri; Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri. Electronic address: mjholtzman@wustl.edu.
Washington University in St. Louis · US

Funding

Defining and Controlling Airway DiseaseR35HL145242 · NHLBI · WASHINGTON UNIVERSITY · PI HOLTZMAN, MICHAEL J · 2019 to 2025
$6.6M
PARP9-DTX3L Control Of Viral Infection and Airway DiseaseR01AI130591 · NIAID · WASHINGTON UNIVERSITY · PI HOLTZMAN, MICHAEL J · 2017 to 2021
$3.0M
NHLBI NIH HHS R35 HL145242NIAID NIH HHS R01 AI130591
6 · The paper itself

Abstract

Respiratory viruses, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), can trigger chronic lung disease that persists and even progresses after expected clearance of infectious virus. To gain an understanding of this process, the current study examined a series of consecutive fatal cases of coronavirus disease 2019 (COVID-19) that came to autopsy at 27 to 51 days after hospital admission. In each patient, a stereotyped bronchiolar-alveolar pattern of lung remodeling was identified with basal epithelial cell hyperplasia, immune activation, and mucinous differentiation. Remodeling regions featured macrophage infiltration and apoptosis and a marked depletion of alveolar type 1 and 2 epithelial cells. This pattern closely resembled findings from an experimental model of post-viral lung disease that requires basal-epithelial stem cell growth, immune activation, and differentiation. Together, these results provide evidence of basal epithelial cell reprogramming in long-term COVID-19 and thereby yield a pathway for explaining and correcting lung dysfunction in this type of disease.

Indexed as

COVID-19Cellular ReprogrammingEpithelial CellsHumansLungSARS-CoV-2

Identifiers

PMID36868468
PMCPMC9977469
OpenAlexW4322753617

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.