Evidence map›Paper›PMID 30879738›Full record

ReviewThe American journal of the medical sciences2019

Metabolic Reprogramming as a Driver of Fibroblast Activation in PulmonaryFibrosis.

Rachel Para, Freddy Romero, Gautam George, Ross Summer

Abstract readReview
In one paragraph

Review in The American journal of the medical sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing 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

34 citing papers in PubMed.

  1. Article
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  9. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
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  19. Identifying Phenotypically Distinct Fibroblast Subsets in Type 2 Diabetes-Associated Iatrogenic Laryngotracheal Stenosis.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2022
    Article
  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.

Rachel ParaDepartment of Medicine, Center for Translational Research and Division of Pulmonary, Allergy and Critical Care Medicine and; Jane & Leonard Korman Respiratory Institute, Thomas Jefferson University, Philadelphia, Pennsylvania.
Freddy RomeroDepartment of Medicine, Center for Translational Research and Division of Pulmonary, Allergy and Critical Care Medicine and; Jane & Leonard Korman Respiratory Institute, Thomas Jefferson University, Philadelphia, Pennsylvania.
Gautam GeorgeDepartment of Medicine, Center for Translational Research and Division of Pulmonary, Allergy and Critical Care Medicine and; Jane & Leonard Korman Respiratory Institute, Thomas Jefferson University, Philadelphia, Pennsylvania.
Ross SummerDepartment of Medicine, Center for Translational Research and Division of Pulmonary, Allergy and Critical Care Medicine and; Jane & Leonard Korman Respiratory Institute, Thomas Jefferson University, Philadelphia, Pennsylvania. Electronic address: ross.summer@jefferson.edu.

Funding

Metabolic control of DNA repair in pulmonary fibrosisR01HL131784 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI SUMMER, ROSS S · 2017 to 2020
$1.6M
PROTEASOME DEGRADATION OF P53 DRIVES HPS LUNG FIBROSISR01HL136833 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI ROMERO, FREDDY · 2018 to 2021
$1.6M
NHLBI NIH HHS R01 HL131784NHLBI NIH HHS R01 HL136833
6 · The paper itself

Abstract

Pulmonary fibrosis refers to a heterogeneous group of disorders that scar the lung, most often irreversibly. To date, there are limited effective treatments for these conditions, despite decades of research in this area of investigation. In pulmonary fibrosis, the principle cell responsible for producing the vast majority of scar tissue is the fibroblast, making these cells ideally suited for drug targeting. For decades, the major experimental approach to blocking the activity of lung fibroblasts has been either to inhibit the interaction of fibroblast growth factors with their receptors or interfere with downstream effector molecules regulating extracellular matrix production. However, emerging evidence now indicates that lung fibroblasts also undergo dramatic metabolic reprogramming in the setting of growth factor stimulation. These discoveries, along with preclinical investigations showing marked reductions in lung fibrosis after targeting specific metabolic pathways, has led to a total rethinking of drug development in the pulmonary fibrosis field. Here, we review the major metabolic pathways and highlight some of the key metabolic events that occur in the transition of fibroblasts from quiescent to activated states. Moreover, we discuss the emerging evidence linking changes in fibroblast metabolism to pulmonary fibrosis and propose how targeting specific metabolic pathways could be employed in the treatment of fibrotic lung diseases.

Indexed as

FibroblastsHumansLungMetabolic Networks and PathwaysPulmonary FibrosisFibroblastGlycolysisLungMetabolismMyofibroblastPulmonary fibrosis

Identifiers

PMID30879738
PMCPMC6478549

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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.