Evidence map›Paper›PMID 42782795›Full record

ReviewCells2026

Developmental Therapeutics for Alveolar Generation and Regeneration: Implications for Bronchopulmonary Dysplasia and Prematurity-Associated Lung Disease.

David Warburton, Rex Moats, Lance A Parton, Edmund F LaGamma, Victoria Niklas

Abstract readReview
In one paragraph

Review in Cells, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

5 authors.

David WarburtonDivision of Newborn Medicine, Maria Fareri Children's Hospital at Westchester Medical Center, Department of Pediatrics, New York Medical College, Boston Children's Health Physicians, Valhalla, NY 10595, USA.
Rex MoatsDevelopmental Biology and Regenerative Medicine Program, Saban Research Institute, Children's Hospital Los Angeles, Keck School of Medicine, University of Southern California, Los Angeles, CA 90027, USA.
Lance A PartonDivision of Newborn Medicine, Maria Fareri Children's Hospital at Westchester Medical Center, Department of Pediatrics, New York Medical College, Boston Children's Health Physicians, Valhalla, NY 10595, USA.
Edmund F LaGammaDivision of Newborn Medicine, Maria Fareri Children's Hospital at Westchester Medical Center, Department of Pediatrics, New York Medical College, Boston Children's Health Physicians, Valhalla, NY 10595, USA.ORCID 0000-0001-9720-1949
Victoria NiklasOak Hill Bio Holdings Ltd., Altrincham WA14 2DT, UK.ORCID 0000-0002-5990-7235

Funding

Oak Hill Bio Holdings Ltd
6 · The paper itself

Abstract

The mechanisms by which alveoli form during lung development remain under investigation. The classical model proposes formation through secondary septation, whereas an alternative proposed model suggests that alveoli arise through epithelial budding within preformed mesenchymal stabilizing rings. Regardless of the precise morphogenetic mechanism, alveolar formation depends on coordinated interactions among epithelial progenitor cells, pulmonary endothelial cells, mesenchymal populations, extracellular matrix remodeling, and biomechanical forces. Stereologic imaging supports continued postnatal alveolar formation and the biological plausibility of alveolar regeneration. These observations are relevant to bronchopulmonary dysplasia (BPD), a disorder of interrupted alveolar and pulmonary vascular development after extremely preterm birth. This review integrates competing morphogenetic models with complementary local and systemic therapeutic concepts. Insulin-like growth factor 1 (IGF-1) provides systemic and local support for alveolar, vascular, and multiorgan maturation. In contrast, fibroblast growth factor 10 (FGF10) is a major local morphogen that regulates epithelial branching, alveolar induction, and repair. Physiologic IGF-1 replacement is being evaluated clinically to reduce BPD severity; FGF10-mediated regeneration remains at the preclinical proof-of-concept stage. Together, these pathways illustrate how preserving or resuming developmental signaling may support lifelong lung health after extremely preterm birth.

Indexed as

Bronchopulmonary DysplasiaPulmonary AlveoliRegenerationAnimalsFibroblast Growth Factor 10HumansInfant, NewbornInfant, PrematureInsulin-Like Growth Factor IFibroblast Growth Factor 10Insulin-Like Growth Factor Ibronchopulmonary dysplasiadevelopmental therapeuticsextremely preterm infantfibroblast growth factor 10insulin-like growth factor-1lungregeneration

Identifiers

PMID42782795
PMCPMC13605248

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.