Evidence map›Paper›PMID 30774991›Full record

ReviewCell death discovery2019

Alveolar type 2 progenitor cells for lung injury repair.

Ayobami Matthew Olajuyin, Xiaoju Zhang, Hong-Long Ji

Open access · goldAbstract readReview
In one paragraph

Review in Cell death discovery, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed
16.9field-weighted citation impact, top 1% 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

125 citing papers in PubMed, 216 citations in OpenAlex.

  1. Article
  2. Novel netrin-1-Unc5b-Klf4 axis balances AT2 survival in experimental bronchopulmonary dysplasia.American journal of respiratory cell and molecular biology · 2026
    Article
  3. Review
  4. Article
  5. Beyond the epithelium: multicellular niches in lung regeneration and disease.American journal of physiology. Lung cellular and molecular physiology · 2026
    Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025
    Review
  20. Article

65 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 2 countries.

Ayobami Matthew Olajuyin1Department of Respiratory Medicine, Henan Provincial People's Hospital, Henan University, Zhengzhou Henan, China.
Xiaoju Zhang1Department of Respiratory Medicine, Henan Provincial People's Hospital, Henan University, Zhengzhou Henan, China.
Hong-Long Ji2Department of Cellular and Molecular Biology, University of Texas Health Science Center at Tyler, Tyler, TX USA.
Henan Provincial People's Hospital · CNHenan University · CNThe University of Texas Health Science Center at Tyler · US

Funding

NOVEL PARACRINE MECHANISMS FOR CELL-BASED THERAPY OF INJURED LUNGSR01HL134828 · NHLBI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI JI, HONG-LONG · 2017 to 2025
$3.4M
NHLBI NIH HHS R01 HL134828
6 · The paper itself

Abstract

Alveolar type 2 progenitor cells (AT2) seem closest to clinical translation, specifying the evidence that AT2 may satisfactorily control the immune response to decrease lung injury by stabilizing host immune-competence and a classic and crucial resource for lung regeneration and repair. AT2 establish potential in benefiting injured lungs. However, significant discrepancies linger in our understanding vis-à-vis the mechanisms for AT2 as a regime for stem cell therapy as well as essential guiding information for clinical trials, including effectiveness in appropriate pre-clinical models, safety, mostly specifications for divergent lung injury patients. These important gaps shall be systematically investigated prior to the vast therapeutic perspective of AT2 cells for pulmonary diseases can be considered. This review focused on AT2 cells homeostasis, pathophysiological changes in the pathogenesis of lung injury, physiological function of AT2 cells, apoptosis of AT2 cells in lung diseases, the role of AT2 cells in repairing processes after lung injury, mechanism of AT2 cells activation promote repairing processes after lung injury, and potential therapy of lung disease by utilizing the AT2 progenitor cells. The advancement remains to causally connect the molecular and cellular alteration of AT2 cells to lung injury and repair. Conclusively, it is identified that AT2 cells can convert into AT1 cells; but, the comprehensive cellular mechanisms involved in this transition are unrevealed. Further investigation is mandatory to determine new strategies to prevent lung injury.

Identifiers

PMID30774991
PMCPMC6368612
OpenAlexW2914134723

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.