Evidence map›Paper›PMID 38501963›Full record

ReviewPhysiology (Bethesda, Md.)2024

Pulmonary Vascular Dysfunctions in Cystic Fibrosis.

Jean-Pierre Amoakon, Goutham Mylavarapu, Raouf S Amin, Anjaparavanda P Naren

Open access · greenAbstract readReview
In one paragraph

Review in Physiology (Bethesda, Md.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

5 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. CFTR as a therapeutic target for severe lung infection.American journal of physiology. Lung cellular and molecular physiology · 2025
    Review
  5. 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

4 authors at 2 institutions in 1 country.

Jean-Pierre AmoakonDepartment of Systems Biology and Physiology, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States.ORCID 0000-0003-1861-2841
Goutham MylavarapuDivision of Pulmonary Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, United States.ORCID 0000-0002-6053-3170
Raouf S AminDivision of Pulmonary Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, United States.ORCID 0000-0002-4942-6024
Anjaparavanda P NarenDepartment of Systems Biology and Physiology, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States.
Cedars-Sinai Medical Center · USCincinnati Children's Hospital Medical Center · US

Funding

Pilot and Feasibility ProgramP30DK117467 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Raouf S. Amin, MICHAEL A. HELMRATH · 2018 to 2026
$11.4M
Inhibition of an apical cAMP transporter (MRP4) in the gut induces diarrheaR01DK080834 · NIDDK · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI Anjaparavanda P Naren · 2009 to 2026
$6.8M
Investigating of the Mechanisms of Action of CFTR Correctors in RescuingDelta F508-CFTRR01HL147351 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI NAREN, ANJAPARAVANDA P · 2020 to 2023
$1.7M
American Heart Association (AHA) 903099HHS | NIH | NHLBI | Division of Intramural Research (DIR) HL147351NHLBI NIH HHS R01 HL147351NIDDK NIH HHS P30 DK117467NIDDK NIH HHS R01 DK080834
6 · The paper itself

Abstract

Cystic fibrosis (CF) is an inherited disorder caused by a deleterious mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Given that the CFTR protein is a chloride channel expressed on a variety of cells throughout the human body, mutations in this gene impact several organs, particularly the lungs. For this very reason, research regarding CF disease and CFTR function has historically focused on the lung airway epithelium. Nevertheless, it was discovered more than two decades ago that CFTR is also expressed and functional on endothelial cells. Despite the great strides that have been made in understanding the role of CFTR in the airway epithelium, the role of CFTR in the endothelium remains unclear. Considering that the airway epithelium and endothelium work in tandem to allow gas exchange, it becomes very crucial to understand how a defective CFTR protein can impact the pulmonary vasculature and overall lung function. Fortunately, more recent research has been dedicated to elucidating the role of CFTR in the endothelium. As a result, several vascular dysfunctions associated with CF disease have come to light. Here, we summarize the current knowledge on pulmonary vascular dysfunctions in CF and discuss applicable therapies.

Indexed as

Cystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorLungAnimalsEndothelium, VascularHumansMutationPulmonary CirculationCFTR protein, humanCystic Fibrosis Transmembrane Conductance RegulatorCFTRcystic fibrosisendothelial barrierendothelial cellspulmonary vasculature

Identifiers

PMID38501963
PMCPMC11368519
OpenAlexW4392953643

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.