Evidence map›Paper›PMID 34023385›Full record

ArticleThe Journal of biological chemistry2021

NOX4 regulates macrophage apoptosis resistance to induce fibrotic progression.

Jennifer L Larson-Casey, Linlin Gu, Jungsoon Kang, Ashish Dhyani, A Brent Carter

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05976217 (Safety and Efficacy of Venetoclax in Idiopathic Pulmonary Fibrosis), which is not on this map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-weighted citation impact, top 11% 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.

NCT05976217 early_phase1completednot on this mapstarted 2023, after this paper: background citation

Safety and Efficacy of Venetoclax in Idiopathic Pulmonary Fibrosis

TypeinterventionalSponsorUniversity of Alabama at BirminghamRan2023 to 2024Enrolled3ConditionsIdiopathic Pulmonary FibrosisArmsVenetoclax
3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Regulated Cell Death in Idiopathic Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  2. Review
  3. Article
  4. Monocyte-mediated mechanisms in idiopathic pulmonary fibrosis: opportunities for early intervention.Apoptosis : an international journal on programmed cell death · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. NOX Dependent ROS Generation and Cell Metabolism.International journal of molecular sciences · 2023
    Review
  14. The role of lung macrophages in acute respiratory distress syndrome.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Review
  15. Review
  16. 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 1 institution in 1 country.

Jennifer L Larson-CaseyDivision of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Linlin GuDivision of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Jungsoon KangDivision of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Ashish DhyaniDivision of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.
A Brent CarterDivision of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA; Birmingham Veterans Administration Medical Center, Birmingham, Alabama, USA. Electronic address: bcarter1@uab.edu.
University of Alabama at Birmingham · US

Funding

ROS Modulation of Innate and Adaptive Immunity in RAP30AR048311 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 2001 to 2017
$9.5M
Project 5 Nano-micro Hybrid Fibrous Materials for Containment Removal and Site RemediationP42ES027723 · NIEHS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LUNGU, CLAUDIU T · 2020 to 2024
$6.7M
Lung Macrophage Metabolic Reprogramming in Asbestos-Induced ToxicityR01ES015981 · NIEHS · UNIVERSITY OF IOWA · PI CARTER, A BRENT · 2007 to 2022
$5.5M
Pulmonary fibrosis is modulated by MCU-mediated macrophage apoptosis resistanceI01CX001715 · VA · BIRMINGHAM VA MEDICAL CENTER · PI CARTER, A BRENT · 2019 to 2023
–
CSRD VA I01 CX001715NIAMS NIH HHS P30 AR048311NIEHS NIH HHS P42 ES027723NIEHS NIH HHS R01 ES015981
6 · The paper itself

Abstract

Pulmonary fibrosis is a progressive lung disease often occurring secondary to environmental exposure. Asbestos exposure is an important environmental mediator of lung fibrosis and remains a significant cause of disease despite strict regulations to limit exposure. Lung macrophages play an integral role in the pathogenesis of fibrosis induced by asbestos (asbestosis), in part by generating reactive oxygen species (ROS) and promoting resistance to apoptosis. However, the mechanism by which macrophages acquire apoptosis resistance is not known. Here, we confirm that macrophages isolated from asbestosis subjects are resistant to apoptosis and show they are associated with enhanced mitochondrial content of NADPH oxidase 4 (NOX4), which generates mitochondrial ROS generation. Similar results were seen in chrysotile-exposed WT mice, while macrophages from Nox4

Indexed as

ApoptosisDisease ProgressionAnimalsbcl-Associated Death ProteinCell LineFemaleIdiopathic Pulmonary FibrosisLungMacrophagesMaleMiceMice, Inbred C57BLMitochondriaModels, BiologicalMonocytesNADPH Oxidase 4bcl-Associated Death ProteinNADPH Oxidase 4Reactive Oxygen Speciesapoptosis resistancemonocyte-derived macrophagesNOX4pulmonary fibrosis

Identifiers

PMID34023385
PMCPMC8214193
OpenAlexW3162814154

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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.