Evidence map›Paper›PMID 38359963›Full record

ArticleThe European respiratory journal2024

Repositioning of ezetimibe for the treatment of idiopathic pulmonary fibrosis.

Chanho Lee, Se Hyun Kwak, Jisu Han, Ju Hye Shin, Byunghun Yoo, Yu Seol Lee, Jeong Su Park, Beom Jin Lim, Jin Gu Lee, Young Sam Kim and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The European respiratory journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
27.2field-weighted citation impact, top 1% 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

8 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Mechanisms and Therapeutic Potential of Myofibroblast Transformation in Pulmonary Fibrosis.Journal of respiratory biology and translational medicine · 2025
    Article
  7. Article
  8. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 1 institution in 1 country.

Chanho LeeDepartment of Biomedical Sciences, Yonsei University College of Medicine, Seoul, Republic of Korea.ORCID https://orcid.org/0000-0003-2065-7379
Se Hyun KwakDivision of Pulmonology, Allergy and Critical Care Medicine, Department of Internal Medicine, Yongin Severance Hospital, Yonsei University College of Medicine, Yongin, Republic of Korea.
Jisu HanDepartment of Biomedical Sciences, Yonsei University College of Medicine, Seoul, Republic of Korea.
Ju Hye ShinDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea.
Byunghun YooDepartment of Biomedical Sciences, Yonsei University College of Medicine, Seoul, Republic of Korea.
Yu Seol LeeDepartment of Biomedical Sciences, Yonsei University College of Medicine, Seoul, Republic of Korea.
Jeong Su ParkDepartment of Biomedical Sciences, Yonsei University College of Medicine, Seoul, Republic of Korea.
Beom Jin LimDepartment of Pathology, Yonsei University College of Medicine, Seoul, Republic of Korea.
Jin Gu LeeDepartment of Thoracic and Cardiovascular Surgery, Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea.
Young Sam KimDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea.
Song Yee KimDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea.
Soo Han BaeDepartment of Biomedical Sciences, Yonsei University College of Medicine, Seoul, Republic of Korea soohanbae@yuhs.ac.
Yonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWe previously identified ezetimibe, an inhibitor of Niemann-Pick C1-like intracellular cholesterol transporter 1 and European Medicines Agency-approved lipid-lowering agent, as a potent autophagy activator. However, its efficacy against pulmonary fibrosis has not yet been evaluated. This study aimed to determine whether ezetimibe has therapeutic potential against idiopathic pulmonary fibrosis.

methodsPrimary lung fibroblasts isolated from both humans and mice were employed for mechanistic

resultsEzetimibe inhibited myofibroblast differentiation by restoring the mechanistic target of rapamycin complex 1-autophagy axis with fine control of intracellular cholesterol distribution. Serum response factor, a potential autophagic substrate, was identified as a primary downstream effector in this process. Similarly, ezetimibe ameliorated bleomycin-induced pulmonary fibrosis in mice by inhibiting mechanistic target of rapamycin complex 1 activity and increasing autophagic flux, as observed in mouse lung samples. Patients with idiopathic pulmonary fibrosis who regularly used ezetimibe showed decreased rates of all-cause mortality and lung function decline.

conclusionOur study presents ezetimibe as a potential novel therapeutic for idiopathic pulmonary fibrosis.

Indexed as

Anticholesteremic AgentsAutophagyDisease Models, AnimalDrug RepositioningEzetimibeIdiopathic Pulmonary FibrosisAgedAnimalsBleomycinCholesterolFemaleFibroblastsHumansLungMaleMiceAnticholesteremic AgentsBleomycinCholesterolEzetimibe

Identifiers

PMID38359963
PMCPMC11096666
OpenAlexW4391836805

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.