Evidence map›Paper›PMID 34621164›Full record

ArticleFrontiers in pharmacology2021

Drug Repurposing Prediction and Validation From Clinical Big Data for the Effective Treatment of Interstitial Lung Disease.

Soni Siswanto, Hiroki Yamamoto, Haruka Furuta, Mone Kobayashi, Takuya Nagashima, Gen Kayanuma, Kazuki Nagayasu, Yumiko Imai, Shuji Kaneko

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.5field-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

6 citing papers in PubMed, 13 citations in OpenAlex.

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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

9 authors at 3 institutions in 1 country.

Soni SiswantoDepartment of Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan.
Hiroki YamamotoDepartment of Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan.
Haruka FurutaDepartment of Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan.
Mone KobayashiDepartment of Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan.
Takuya NagashimaDepartment of Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan.
Gen KayanumaDepartment of Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan.
Kazuki NagayasuDepartment of Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan.
Yumiko ImaiLaboratory of Regulation of Intractable Infectious Diseases, National Institutes of Biomedical Innovation Health and Nutrition, Osaka, Japan.
Shuji KanekoDepartment of Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan.
Kyoto University · JPKyoto Pharmaceutical University · JPNational Institute of Biomedical Innovation, Health and Nutrition · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interstitial lung diseases (ILDs) are a group of respiratory disorders characterized by chronic inflammation and fibrosis of the pulmonary interstitial tissues. Although the etiology of ILD remains unclear, some drug treatments are among the primary causes of ILD. In the present study, we analyzed the FDA Adverse Event Reporting System and JMDC Inc. insurance claims to identify a coexisting drug that reduced the incidence of ILD associated with the use of an anti-arrhythmic agent, amiodarone, and found that the thrombin inhibitor dabigatran prevented the amiodarone-induced ILD in both clinical datasets. In an experimental validation of the hypothesis, long-term oral treatment of mice with amiodarone caused a gradual decrease in body weight caused by respiratory insufficiency. In the lungs of amiodarone-treated mice, infiltration of macrophages was observed in parallel with a delayed upregulation of the platelet-derived growth factor receptor α gene. In contrast, co-treatment with dabigatran significantly attenuated these amiodarone-induced changes indicative of ILD. These results suggest that dabigatran is effective in preventing drug-induced ILD. This combinatorial approach of drug repurposing based on clinical big data will pave the way for finding a new treatment with high clinical predictability and a well-defined molecular mechanism.

Indexed as

adverse eventamiodaronechronic inflammationdabigatranpulmonary fibrosisreal-world dataretrospective analysis

Identifiers

PMID34621164
PMCPMC8490809
OpenAlexW3199499380

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.