Evidence map›Paper›PMID 36573684›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2023

The matricellular protein CCN3 supports lung endothelial homeostasis and function.

Kalpana R Betageri, Patrick A Link, Andrew J Haak, Giovanni Ligresti, Daniel J Tschumperlin, Nunzia Caporarello

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. The advance of CCN3 in fibrosis.Journal of cell communication and signaling · 2023
    Review
  8. The vascular perspective on acute and chronic lung disease.The Journal of clinical investigation · 2023
    Review
  9. CCN proteins: opportunities for clinical studies-a personal perspective.Journal of cell communication and signaling · 2023
    Review
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

6 authors at 1 institution in 1 country.

Kalpana R BetageriDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota.ORCID 0000-0003-1320-8313
Patrick A LinkDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota.ORCID 0000-0003-1847-8857
Andrew J HaakDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota.ORCID 0000-0002-5323-253X
Giovanni LigrestiDepartment of Medicine, Boston University School of Medicine, Boston, Massachusetts.
Daniel J TschumperlinDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota.ORCID 0000-0002-5115-9025
Nunzia CaporarelloDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota.ORCID 0000-0002-3183-2868
Mayo Clinic · US

Funding

Mechanobiology of Lung FibrosisR01HL092961 · NHLBI · MAYO CLINIC ROCHESTER · PI Daniel J. Tschumperlin · 2009 to 2026
$8.0M
Interdisciplinary Training in Lung Physiology and Biomedical EngineeringT32HL105355 · NHLBI · MAYO CLINIC ROCHESTER · PI PRAKASH, Y. S., SIECK, GARY C. · 2012 to 2021
$3.9M
Epigenetic regulation of pulmonary fibrosisR01HL142596 · NHLBI · MAYO CLINIC ROCHESTER · PI Giovanni Ligresti · 2018 to 2026
$2.9M
Targeting vascular dysfunction to promote lung repair and fibrosis resolutionR01HL158733 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LIGRESTI, GIOVANNI · 2022 to 2025
$2.8M
Targeting CEBPA To Restore Epithelial-Mesenchymal Homeostasis In Lung FibrosisR01HL153026 · NHLBI · UNIVERSITY OF MINNESOTA · PI TAN, QI · 2020 to 2024
$2.3M
Targeting redox to resorb ECMF32HL158018 · NHLBI · MAYO CLINIC ROCHESTER · PI LINK, PATRICK · 2022 to 2022
$68k
NHLBI NIH HHS F32 HL158018NHLBI NIH HHS L30 HL159704NHLBI NIH HHS R01 HL092961NHLBI NIH HHS R01 HL142596NHLBI NIH HHS R01 HL153026NHLBI NIH HHS R01 HL158733NHLBI NIH HHS T32 HL105355
6 · The paper itself

Abstract

Aberrant vascular remodeling contributes to the progression of many aging-associated diseases, including idiopathic pulmonary fibrosis (IPF), where heterogeneous capillary density, endothelial transcriptional alterations, and increased vascular permeability correlate with poor disease outcomes. Thus, identifying disease-driving mechanisms in the pulmonary vasculature may be a promising strategy to limit IPF progression. Here, we identified

Indexed as

Pulmonary FibrosisAnimalsCells, CulturedEndothelial CellsHumansLungMiceNephroblastoma Overexpressed ProteinNephroblastoma Overexpressed ProteinCCN3idiopathic pulmonary fibrosislung homeostasispulmonary fibrosispulmonary vasculature

Identifiers

PMID36573684
PMCPMC9925165
OpenAlexW4312211712

What Socratic 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 Socratic graph.