Evidence map›Paper›PMID 27790277›Full record

ArticleTuberculosis and respiratory diseases2016

Increased Cellular NAD

Gi-Su Oh, Su-Bin Lee, Anjani Karna, Hyung-Jin Kim, AiHua Shen, Arpana Pandit, SeungHoon Lee, Sei-Hoon Yang, Hong-Seob So

Open access · diamondAbstract read
In one paragraph

Article in Tuberculosis and respiratory diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 34 citations in OpenAlex.

  1. A Redox-Shifted Fibroblast Subpopulation Emerges in the Fibrotic Lung.American journal of respiratory cell and molecular biology · 2024
    Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Loss of ANT1 Increases Fibrosis and Epithelial Cell Senescence in Idiopathic Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. 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

9 authors at 1 institution in 1 country.

Gi-Su OhDepartment of Microbiology, Center for Metabolic Function Regulation, Wonkwang University School of Medicine, Iksan, Korea.
Su-Bin LeeDepartment of Microbiology, Center for Metabolic Function Regulation, Wonkwang University School of Medicine, Iksan, Korea.
Anjani KarnaDepartment of Microbiology, Center for Metabolic Function Regulation, Wonkwang University School of Medicine, Iksan, Korea.
Hyung-Jin KimDepartment of Microbiology, Center for Metabolic Function Regulation, Wonkwang University School of Medicine, Iksan, Korea.
AiHua ShenDepartment of Microbiology, Center for Metabolic Function Regulation, Wonkwang University School of Medicine, Iksan, Korea.
Arpana PanditDepartment of Microbiology, Center for Metabolic Function Regulation, Wonkwang University School of Medicine, Iksan, Korea.
SeungHoon LeeDepartment of Microbiology, Center for Metabolic Function Regulation, Wonkwang University School of Medicine, Iksan, Korea.
Sei-Hoon YangDepartment of Internal Medicine, Wonkwang University School of Medicine, Iksan, Korea.
Hong-Seob SoDepartment of Microbiology, Center for Metabolic Function Regulation, Wonkwang University School of Medicine, Iksan, Korea.
Wonkwang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIdiopathic pulmonary fibrosis is a common interstitial lung disease; it is a chronic, progressive, and fatal lung disease of unknown etiology. Over the last two decades, knowledge about the underlying mechanisms of pulmonary fibrosis has improved markedly and facilitated the identification of potential targets for novel therapies. However, despite the large number of antifibrotic drugs being described in experimental pre-clinical studies, the translation of these findings into clinical practices has not been accomplished yet. NADH:quinone oxidoreductase 1 (NQO1) is a homodimeric enzyme that catalyzes the oxidation of NADH to NAD

methodsC57BL/6 mice were treated with intratracheal instillation of bleomycin. The mice were orally administered with β-lapachone from 3 days before exposure to bleomycin to 1-3 weeks after exposure to bleomycin. Bronchoalveolar lavage fluid (BALF) was collected for analyzing the infiltration of immune cells. In vitro, A549 cells were treated with transforming growth factor β1 (TGF-β1) and β-lapachone to analyze the extracellular matrix (ECM) and epithelial-mesenchymal transition (EMT).

resultsβ-Lapachone strongly attenuated bleomycin-induced lung inflammation and fibrosis, characterized by histological staining, infiltrated immune cells in BALF, inflammatory cytokines, fibrotic score, and TGF-β1, α-smooth muscle actin accumulation. In addition, β-lapachone showed a protective role in TGF-β1-induced ECM expression and EMT in A549 cells.

conclusionOur results suggest that β-lapachone can protect against bleomycin-induced lung inflammation and fibrosis in mice and TGF-β1-induced EMT in vitro, by elevating the NAD

Indexed as

CellFibrosisInflammationMiceNADNQO1 Protein, HumanPulmonary FibrosisTransforming Growth Factor Beta1

Identifiers

PMID27790277
PMCPMC5077729
OpenAlexW2533146992

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.