Evidence map›Paper›PMID 31928788›Full record

ReviewRedox biology2020

Mitochondrial quality control in pulmonary fibrosis.

Jennifer L Larson-Casey, Chao He, A Brent Carter

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
14.2field-weighted citation impact, top 1% 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

97 citing papers in PubMed, 201 citations in OpenAlex.

  1. Article
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  15. Review
  16. Altered Metabolism in Idiopathic Pulmonary Fibrosis.Journal of cellular physiology · 2025
    Review
  17. Article
  18. Article
  19. Article
  20. Article

37 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Jennifer L Larson-CaseyDepartment of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, AL, 35294, United States.
Chao HeDepartment of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, AL, 35294, United States.
A Brent CarterDepartment of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, AL, 35294, United States; Birmingham VAMC, Birmingham, AL, 35294, United States. Electronic address: bcarter1@uab.edu.
University of Alabama at Birmingham · USBirmingham VA Medical Center · US

Funding

Therapeutic Targeting of the Myofibroblast in Fibrotic Lung DiseaseP01HL114470 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI THANNICKAL, VICTOR J. · 2013 to 2022
$17.8M
Lung Macrophage Metabolic Reprogramming in Asbestos-Induced ToxicityR01ES015981 · NIEHS · UNIVERSITY OF IOWA · PI CARTER, A BRENT · 2007 to 2022
$5.5M
Training Program in Lung Biology and Translational MedicineT32HL105346 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GAGGAR, AMIT · 2010 to 2025
$5.0M
Pulmonary fibrosis is modulated by MCU-mediated macrophage apoptosis resistanceI01CX001715 · VA · BIRMINGHAM VA MEDICAL CENTER · PI CARTER, A BRENT · 2019 to 2023
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CSRD VA I01 CX001715NHLBI NIH HHS P01 HL114470NHLBI NIH HHS T32 HL105346NIEHS NIH HHS R01 ES015981
6 · The paper itself

Abstract

Mechanisms underlying the pathogenesis of pulmonary fibrosis remain incompletely understood. Emerging evidence suggests changes in mitochondrial quality control are a critical determinant in many lung diseases, including chronic obstructive pulmonary disease, asthma, pulmonary hypertension, acute lung injury, lung cancer, and in the susceptibility to pulmonary fibrosis. Once thought of as the kidney-bean shaped powerhouses of the cell, mitochondria are now known to form interconnected networks that rapidly and continuously change their size to meet cellular metabolic demands. Mitochondrial quality control modulates cell fate and homeostasis, and diminished mitochondrial quality control results in mitochondrial dysfunction, increased reactive oxygen species (ROS) production, reduced ATP production, and often induces intrinsic apoptosis. Here, we review the role of the mitochondria in alveolar epithelial cells, lung macrophages, and fibroblasts within the context of pulmonary fibrosis.

Indexed as

MitochondriaPulmonary FibrosisAlveolar Epithelial CellsApoptosisHumansReactive Oxygen SpeciesReactive Oxygen Species

Identifiers

PMID31928788
PMCPMC7251238
OpenAlexW3000348775

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.