Evidence map›Paper›PMID 24625972›Full record

ArticleCell death & disease2014

BAX inhibitor-1-associated V-ATPase glycosylation enhances collagen degradation in pulmonary fibrosis.

M-R Lee, G-H Lee, H-Y Lee, D-S Kim, M J Chung, Y C Lee, H-R Kim, H-J Chae

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

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  14. Downregulation of RUVBL1 inhibits proliferation of lung adenocarcinoma cells by G1/S phase cell cycle arrest via multiple mechanisms.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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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

8 authors at 2 institutions in 1 country.

M-R LeeDepartment of Pharmacology and Institute of Cardiovascular Research, Medical School, Chonbuk National University, Jeonju, Chonbuk, Republic of Korea.
G-H LeeDepartment of Pharmacology and Institute of Cardiovascular Research, Medical School, Chonbuk National University, Jeonju, Chonbuk, Republic of Korea.
H-Y LeeDepartment of Pharmacology and Institute of Cardiovascular Research, Medical School, Chonbuk National University, Jeonju, Chonbuk, Republic of Korea.
D-S KimDepartment of Pharmacology and Institute of Cardiovascular Research, Medical School, Chonbuk National University, Jeonju, Chonbuk, Republic of Korea.
M J ChungDepartment of Pathology, Chonbuk National University Medical School, Jeonju, Chonbuk, Republic of Korea.
Y C LeeDepartment of Internal Medicine, Chonbuk National University, Medical School, Jeonju, Chonbuk, Republic of Korea.
H-R KimDepartment of Dental Pharmacology, School of Dentistry, Wonkwang University, Iksan, Chonbuk, Republic of Korea.
H-J ChaeDepartment of Pharmacology and Institute of Cardiovascular Research, Medical School, Chonbuk National University, Jeonju, Chonbuk, Republic of Korea.
Jeonbuk National University · KRWonkwang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endoplasmic reticulum (ER) stress is considered one of the pathological mechanisms of idiopathic pulmonary fibrosis (IPF). Therefore, we examined whether an ER stress regulator, Bax inhibitor-1 (BI-1), regulates collagen accumulation, which is both a marker of fibrosis and a pathological mechanism of fibrosis. The presence of BI-1 inhibited the transforming growth factor-β1-induced epithelial-mesenchymal transition of epithelial pulmonary cells and bleomycin-induced pulmonary fibrosis in a mouse model by enhancing collagen degradation, most likely by enhanced activation of the lysosomal V-ATPase through glycosylation. We also found a correlation between post-translational glycosylation of the V-ATPase and its associated chaperone, calnexin, in BI-1-overexpressing cells. BI-1-induced degradation of collagen through lysosomal V-ATPase glycosylation and the involvement of calnexin were confirmed in a bleomycin-induced fibrosis mouse model. These results highlight the regulatory role of BI-1 in IPF and reveal for the first time the role of lysosomal V-ATPase glycosylation in IPF.

Indexed as

Protein Processing, Post-TranslationalAnimalsApoptosis Regulatory ProteinsBleomycinCalnexinCalreticulinCell Line, TumorCollagenDisease Models, AnimalEndoplasmic Reticulum StressEnzyme ActivationEpithelial CellsEpithelial-Mesenchymal TransitionGlycosylationHumansLungApoptosis Regulatory ProteinsBleomycinCalnexinCalreticulinCollagenMembrane ProteinsTGFB1 protein, humanTMBIM6 protein, humanTmbim6 protein, mouseTransforming Growth Factor beta1Vacuolar Proton-Translocating ATPases

Identifiers

PMID24625972
PMCPMC3973240
OpenAlexW2044819472

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.