Evidence map›Paper›PMID 31940218›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2020

TNFα selectively activates the IRE1α/XBP1 endoplasmic reticulum stress pathway in human airway smooth muscle cells.

John Yap, Xujiao Chen, Philippe Delmotte, Gary C Sieck

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

38 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Review
  3. Molecular mechanisms underlying FCCP-induced mitophagy in human airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
  4. Article
  5. Tumor necrosis factor α-induced endoplasmic reticulum stress promotes airway smooth muscle cell proliferation.American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
  6. Article
  7. Article
  8. TNFα-mediated subcellular heterogeneity of succinate dehydrogenase activity in human airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2025
    Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Molecular mechanisms underlying TNFα-induced mitochondrial fragmentation in human airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  17. Article
  18. Review
  19. Article
  20. Understanding the impact of ER stress on lung physiology.Frontiers in cell and developmental biology · 2024
    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 at 1 institution in 1 country.

John YapDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota.
Xujiao ChenDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota.
Philippe DelmotteDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota.
Gary C SieckDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota.
Mayo Clinic · US

Funding

Role of Mitochondria in Airway Smooth MuscleR01HL126451 · NHLBI · MAYO CLINIC ROCHESTER · PI PRAKASH, Y. S., SIECK, GARY C. · 2015 to 2018
$1.9M
NHLBI NIH HHS R01 HL126451
6 · The paper itself

Abstract

Airway inflammation is a key aspect of diseases such as asthma. Proinflammatory cytokines such as TNFα mediate the inflammatory response. In various diseases, inflammation leads to endoplasmic reticulum (ER) stress, the accumulation of unfolded proteins, which triggers homeostatic responses to restore normal cellular function. We hypothesized that TNFα triggers ER stress through an increase in reactive oxygen species generation in human airway smooth muscle (hASM) with a downstream effect on mitofusin 2 (Mfn2). In hASM cells isolated from lung specimens incidental to patient surgery, dose- and time-dependent effects of TNFα exposure were assessed. Exposure of hASM to tunicamycin was used as a positive control. Tempol (500 μM) was used as superoxide scavenger. Activation of three ER stress pathways were evaluated by Western blotting:

Indexed as

Cells, CulturedeIF-2 KinaseEndoplasmic ReticulumEndoplasmic Reticulum StressEndoribonucleasesEukaryotic Initiation Factor-2HumansMuscle, Smooth, VascularPhosphorylationProtein Serine-Threonine KinasesSignal TransductionTumor Necrosis Factor-alphaUnfolded Protein ResponseX-Box Binding Protein 1EIF2AK3 protein, humaneIF-2 KinaseEndoribonucleasesERN1 protein, humanEukaryotic Initiation Factor-2Protein Serine-Threonine KinasesTNF protein, humanTumor Necrosis Factor-alphaX-Box Binding Protein 1XBP1 protein, humanairway smooth muscleasthmaER stressinflammationTNFα

Identifiers

PMID31940218
PMCPMC7099431
OpenAlexW2999224408

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.