Evidence map›Paper›PMID 33208169›Full record

ReviewRespiratory research2020

Pulmonary hypertension secondary to pulmonary fibrosis: clinical data, histopathology and molecular insights.

Grégoire Ruffenach, Jason Hong, Mylène Vaillancourt, Lejla Medzikovic, Mansoureh Eghbali

Open access · goldAbstract readReview
In one paragraph

Review in Respiratory research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
4.9field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 85 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. KPharmaceuticals (Basel, Switzerland) · 2026
    Review
  6. Article
  7. Review
  8. Review
  9. The intersection of liver cirrhosis and pulmonary fibrosis.Journal of translational medicine · 2025
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Succinate aggravates pulmonary fibrosis through the succinate/SUCNR1 axis.American journal of physiology. Lung cellular and molecular physiology · 2025
    Article
  17. Veterinary sciences · 2025
    Article
  18. Article
  19. Article
  20. 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

5 authors at 2 institutions in 1 country.

Grégoire RuffenachDivision of Molecular Medicine, Department of Anesthesiology and Perioperiative Medicine, David Geffen School of Medicine, University of California, BH-550CHS, Los Angeles, CA, 90095-7115, USA.ORCID http://orcid.org/0000-0001-6419-4332
Jason HongDivision of Molecular Medicine, Department of Anesthesiology and Perioperiative Medicine, David Geffen School of Medicine, University of California, BH-550CHS, Los Angeles, CA, 90095-7115, USA.
Mylène VaillancourtDepartment of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Lejla MedzikovicDivision of Molecular Medicine, Department of Anesthesiology and Perioperiative Medicine, David Geffen School of Medicine, University of California, BH-550CHS, Los Angeles, CA, 90095-7115, USA.
Mansoureh EghbaliDivision of Molecular Medicine, Department of Anesthesiology and Perioperiative Medicine, David Geffen School of Medicine, University of California, BH-550CHS, Los Angeles, CA, 90095-7115, USA. meghbali@ucla.edu.
University of California, Los Angeles · USCedars-Sinai Medical Center · US

Funding

Role of miR193 in oxidized lipid induced pulmonary hypertensionR01HL129051 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI EGHBALI, MANSOUREH, REDDY, SRINIVASA T. · 2016 to 2019
$2.3M
Role of miR125 in pulmonary hypertension secondary to interstitial lung diseaseR01HL147586 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI EGHBALI, MANSOUREH · 2020 to 2023
$1.9M
American Heart Association 20POST35210727NHLBI NIH HHS R01 HL129051NHLBI NIH HHS R01 HL147586NIH HHS R01HL129051NIH HHS R01HL147586
6 · The paper itself

Abstract

Pulmonary hypertension (PH) developing secondarily in pulmonary fibrosis (PF) patients (PF-PH) is a frequent co-morbidity. The high prevalence of PH in PF patients is very concerning since the presence of PH is a strong predictor of mortality in PF patients. Until recently, PH was thought to arise solely from fibrotic destruction of the lung parenchyma, leading to hypoxic vasoconstriction and loss of vascular bed density. Thus, potential cellular and molecular dysregulation of vascular remodeling as a driver of PF-PH has been under-investigated. The recent demonstrations that there is no correlation between the severity of the fibrosis and development of PH, along with the finding that significant vascular histological and molecular differences exist between patients with and without PH have shifted the etiological paradigm of PF-PH. This review aims to provide a comprehensive translational overview of PH in PF patients from clinical diagnosis and outcome to the latest understanding of the histology and molecular pathophysiology of PF-PH.

Indexed as

AnimalsEchocardiographyHumansHypertension, PulmonaryInflammation MediatorsLungPulmonary FibrosisRespiratory Function TestsVascular RemodelingInflammation MediatorsPulmonary fibrosisPulmonary hypertensionVascular diseases

Identifiers

PMID33208169
PMCPMC7677848
OpenAlexW3106226515

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.