Evidence map›Paper›PMID 40331514›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2025

Development of novel technology for the visualization and quantitation of angiogenesis and the alveolar-capillary network in a mouse model of fibrosis.

Hannah F Thorndyke, Evan P Lundberg, Edwin Ortiz Gaxon, Maggie M Dawson, Emma C Mason, Julia M Hollaway, Eszter K Vladar, David Coronado Escobar, Susan M Majka

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

9 authors.

Hannah F ThorndykeDivision of Pulmonary, Critical Care & Sleep Medicine, Department of Medicine, National Jewish Health, Denver, Colorado, United States.
Evan P LundbergDivision of Pulmonary, Critical Care & Sleep Medicine, Department of Medicine, National Jewish Health, Denver, Colorado, United States.ORCID 0009-0002-6280-1076
Edwin Ortiz GaxonCell, Stem Cell and Development Graduate Program, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States.
Maggie M DawsonDivision of Pulmonary, Critical Care & Sleep Medicine, Department of Medicine, National Jewish Health, Denver, Colorado, United States.
Emma C MasonDivision of Pulmonary, Critical Care & Sleep Medicine, Department of Medicine, National Jewish Health, Denver, Colorado, United States.
Julia M HollawayDivision of Pulmonary, Critical Care & Sleep Medicine, Department of Medicine, National Jewish Health, Denver, Colorado, United States.
Eszter K VladarDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States.ORCID 0000-0002-4160-8894
David Coronado EscobarOnimagin Technologies SCA, Cordoba, Spain.
Susan M MajkaDivision of Pulmonary, Critical Care & Sleep Medicine, Department of Medicine, National Jewish Health, Denver, Colorado, United States.ORCID 0000-0002-1005-1552

Funding

Mesenchymal Vascular Progenitor Depletion Promotes Lung Aging and Susceptibility to EmphysemaR35HL161238 · NHLBI · NATIONAL JEWISH HEALTH · PI SUSAN M MAJKA · 2022 to 2026
$4.9M
Loss of progenitor function accelerates lung agingR01AG073317 · NIA · NATIONAL JEWISH HEALTH · PI SUSAN M MAJKA, Richard Lee Reinhardt · 2023 to 2026
$2.7M
Canonical to noncanonical Wnt signaling switch in airway epithelial health and diseaseR01HL166895 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI Eszter Katalin Vladar · 2024 to 2026
$1.9M
Loss of progenitor function accelerates lung agingR56AG073317 · NIA · NATIONAL JEWISH HEALTH · PI MAJKA, SUSAN M, REINHARDT, RICHARD LEE · 2021 to 2021
$336k
HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) R35HL161238HHS | NIH | National Institute on Aging (NIA) R56AG073317/RAG073317NHLBI NIH HHS R01 HL166895NHLBI NIH HHS R35 HL161238NIA NIH HHS R01 AG073317NIA NIH HHS R56 AG073317
6 · The paper itself

Abstract

Adaptive angiogenesis can drive repair or underlie the pathogenesis of tissue remodeling. Pulmonary vascular dysfunction is a major manifestation of chronic lung disease (CLD), but the role of angiogenesis in the development of CLD is not well defined. Microvascular capillaries in the alveolar-capillary network are the vessels most affected by pruning and remodeling in the lung, resulting in reduced capillary length and diameter with subsequent loss of gas exchange surfaces. Our lab has previously demonstrated that microvascular endothelial progenitor cells (mvEPCs) drive reparative angiogenesis. We hypothesize that visualization of the alveolar-capillary microvasculature in three-dimensions is essential to define the mechanisms governing repair versus progression to the pathogenesis of CLD. To address this gap in knowledge, we have developed a simple and reliable fluorescent perfusion technique that will allow the quantitation of microvessel structure in the alveolar-capillary network using mouse models of lung injury. This approach may be used in various organ systems to visualize microvasculature structure and its role in disease.

Indexed as

CapillariesNeovascularization, PathologicPulmonary AlveoliPulmonary FibrosisAngiogenesisAnimalsDisease Models, AnimalEndothelial Progenitor CellsMiceMice, Inbred C57BLMicrovesselsalveolar-capillary networkATP binding cassette subfamily G member 2 (ABCG2)fibrosismicrovascular endothelial progenitor cell (mvEPC)reparative angiogenesis

Identifiers

PMID40331514
PMCPMC12342665

What OpenQuestion holds

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Registered trials

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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.