Evidence map›Paper›PMID 38117250›Full record

ArticleAmerican journal of respiratory cell and molecular biology2024

BCL-2 Modulates IRE1α Activation to Attenuate Endoplasmic Reticulum Stress and Pulmonary Fibrosis.

Claude Jourdan Le Saux, Tsung Che Ho, Alexis M Brumwell, Jaymin J Kathiriya, Ying Wei, Jun-Wei B Hughes, Kiana Garakani, Kamran Atabai, Vincent C Auyeung, Ferroz R Papa and 1 more

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.5field-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.

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

13 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
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  6. Mechanisms and markers of lung ageing in health and disease.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  7. Article
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  10. Review
  11. Article
  12. Article
  13. Getting the Timing Right: Controlling BCL-2 Inhibition as an Antifibrotic Therapy.American journal of respiratory cell and molecular biology · 2024
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Claude Jourdan Le SauxDivision of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, California; and.ORCID 0000-0002-6041-2870
Tsung Che HoDivision of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, California; and.
Alexis M BrumwellDivision of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, California; and.
Jaymin J KathiriyaDivision of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, California; and.
Ying WeiDivision of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, California; and.
Jun-Wei B HughesBuck Institute for Research on Aging, Novato, California.
Kiana GarakaniDivision of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, California; and.
Kamran AtabaiDivision of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, California; and.
Vincent C AuyeungDivision of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, California; and.
Ferroz R PapaDivision of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, California; and.
Harold A ChapmanDivision of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, California; and.
University of California, San Francisco · USBuck Institute for Research on Aging · US

Funding

Epithelial stem/progenitor cells as repair agents in diffuse alveolar damageU01HL134766 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHAPMAN, HAROLD A, KOTTON, DARRELL N. · 2016 to 2022
$8.1M
Program to promote lung regeneration and block fibrosisR35HL150767 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHAPMAN, HAROLD A · 2020 to 2025
$5.8M
REGULATION OF INTEGRIN FUNCTIONR01HL044712 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHAPMAN, HAROLD A · 1991 to 2014
$4.8M
Interventional Targeting of the IRE1alpha-TGFbeta signaling loop in pulmonary fibrosisR01HL145037 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PAPA, FEROZ R, SHEPPARD, DEAN · 2019 to 2022
$3.0M
IRE1α mediated dysregulation of the pulmonary epithelium in lung fibrosisK08HL157654 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI AUYEUNG, VINCENT CHURK-MAN · 2021 to 2025
$874k
Sources and Regulation of Epithelial Stem/Progenitor Cells in Alveolar RegenerationR00HL155785 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI KATHIRIYA, JAYMIN J · 2023 to 2025
$747k
Sources and Regulation of Epithelial Stem/Progenitor Cells in Alveolar RegenerationK99HL155785 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KATHIRIYA, JAYMIN J · 2021 to 2022
$315k
NHLBI NIH HHS K08 HL157654NHLBI NIH HHS K99 HL155785NHLBI NIH HHS R00 HL155785NHLBI NIH HHS R01 HL044712NHLBI NIH HHS R01 HL145037NHLBI NIH HHS R35 HL150767NHLBI NIH HHS U01 HL134766
6 · The paper itself

Abstract

BCL-2 family members are known to be implicated in survival in numerous biological settings. Here, we provide evidence that in injury and repair processes in lungs, BCL-2 mainly acts to attenuate endoplasmic reticulum (ER) stress and limit extracellular matrix accumulation. Days after an intratracheal bleomycin challenge, mice lose a fraction of their alveolar type II epithelium from terminal ER stress driven by activation of the critical ER sensor and stress effector IRE1α. This fraction is dramatically increased by BCL-2 inhibition, because IRE1α activation is dependent on its physical association with the BCL-2-proapoptotic family member BAX, and we found BCL-2 to disrupt this association

Indexed as

Aniline CompoundsPulmonary FibrosisSulfonamidesAnimalsBleomycinCollagenEndoplasmic Reticulum StressEndoribonucleasesMiceMice, KnockoutProtein Serine-Threonine KinasesAniline CompoundsBleomycinCollagenEndoribonucleasesnavitoclaxProtein Serine-Threonine KinasesSulfonamidesalveolar epithelial cellsBcl-2ER stressfibroblastfibrosis

Identifiers

PMID38117250
PMCPMC11478128
OpenAlexW4389993018

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.