Evidence map›Paper›PMID 38891046›Full record

ReviewCells2024

Fibroblasts in Pulmonary Hypertension: Roles and Molecular Mechanisms.

Hui Zhang, Min Li, Cheng-Jun Hu, Kurt R Stenmark

Abstract readReview
In one paragraph

Review in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. The emerging role of integrin signaling in pulmonary vascular disease.American journal of physiology. Lung cellular and molecular physiology · 2026
    Review
  7. Article
  8. Review
  9. Mechanisms Underlying Altitude-Induced and Group 3 Pulmonary Hypertension.International journal of molecular sciences · 2026
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Vascular Remodeling: The Multicellular Mechanisms of Pulmonary Hypertension.International journal of molecular sciences · 2025
    Review
  20. 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

4 authors.

Hui ZhangCardiovascular Pulmonary Research Laboratories, Departments of Pediatrics and Medicine, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, CO 80045, USA.
Min LiCardiovascular Pulmonary Research Laboratories, Departments of Pediatrics and Medicine, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, CO 80045, USA.
Cheng-Jun HuCardiovascular Pulmonary Research Laboratories, Departments of Pediatrics and Medicine, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, CO 80045, USA.ORCID 0000-0003-0985-1285
Kurt R StenmarkCardiovascular Pulmonary Research Laboratories, Departments of Pediatrics and Medicine, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, CO 80045, USA.ORCID 0000-0001-6918-6411

Funding

Role of Complement-Driven Pulmonary Vascular Inflammation in PHP01HL152961 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI DELANEY, CASSIDY A · 2020 to 2024
$14.1M
CSRD VA 1NHLBI NIH HHS P01 HL152961NIH HHS 1P01HL152961-01A1U.S. Department of Defense W81XWH1910259U.S. Department of Defense W81XWH2010249
6 · The paper itself

Abstract

Fibroblasts, among the most prevalent and widely distributed cell types in the human body, play a crucial role in defining tissue structure. They do this by depositing and remodeling extracellular matrixes and organizing functional tissue networks, which are essential for tissue homeostasis and various human diseases. Pulmonary hypertension (PH) is a devastating syndrome with high mortality, characterized by remodeling of the pulmonary vasculature and significant cellular and structural changes within the intima, media, and adventitia layers. Most research on PH has focused on alterations in the intima (endothelial cells) and media (smooth muscle cells). However, research over the past decade has provided strong evidence of the critical role played by pulmonary artery adventitial fibroblasts in PH. These fibroblasts exhibit the earliest, most dramatic, and most sustained proliferative, apoptosis-resistant, and inflammatory responses to vascular stress. This review examines the aberrant phenotypes of PH fibroblasts and their role in the pathogenesis of PH, discusses potential molecular signaling pathways underlying these activated phenotypes, and highlights areas of research that merit further study to identify promising targets for the prevention and treatment of PH.

Indexed as

FibroblastsHypertension, PulmonaryAnimalsHumansPulmonary ArterySignal Transductionadventitial fibroblastepigeneticsgene regulationhypoxiainflammationmetabolismmitochondrialpulmonary arterial hypertensionvascular remodeling

Identifiers

PMID38891046
PMCPMC11171669

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.