Evidence map›Paper›PMID 38132116›Full record

ArticleCells2023

Daphnetin Alleviates Bleomycin-Induced Pulmonary Fibrosis through Inhibition of Epithelial-to-Mesenchymal Transition and IL-17A.

Soo-Jin Park, Hyung Won Ryu, Ji-Hyeong Kim, Hwa-Jeong Hahn, Hyun-Jae Jang, Sung-Kyun Ko, Sei-Ryang Oh, Hyun-Jun Lee

Open access · goldAbstract read
In one paragraph

Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

15 citing papers in PubMed, 15 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

8 authors at 1 institution in 1 country.

Soo-Jin ParkNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju-si 28116, Republic of Korea.ORCID 0000-0002-9304-4840
Hyung Won RyuNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju-si 28116, Republic of Korea.ORCID 0000-0001-5291-3942
Ji-Hyeong KimNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju-si 28116, Republic of Korea.ORCID 0009-0004-7933-0682
Hwa-Jeong HahnNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju-si 28116, Republic of Korea.
Hyun-Jae JangNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju-si 28116, Republic of Korea.ORCID 0000-0002-4383-4465
Sung-Kyun KoDepartment of Biomolecular Science, University of Science & Technology (UST), Daejeon 34113, Republic of Korea.ORCID 0000-0002-8202-1205
Sei-Ryang OhNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju-si 28116, Republic of Korea.ORCID 0000-0002-9769-4779
Hyun-Jun LeeNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju-si 28116, Republic of Korea.ORCID 0000-0003-1293-6159
Korea Research Institute of Bioscience and Biotechnology · KR

Funding

Korea Research Institute of Bioscience and Biotechnology KGM5522322National Research Foundation of Korea NRF-2021R1A2C2009624National Research Foundation of Korea RS-2023-00213076
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic and refractory interstitial lung disease. Although there is no cure for IPF, the development of drugs with improved efficacy in the treatment of IPF is required. Daphnetin, a natural coumarin derivative, has immunosuppressive, anti-inflammatory, and antioxidant activities. However, its antifibrotic effects have not yet been elucidated. In this study, we investigated the antifibrotic effects of daphnetin on pulmonary fibrosis and the associated molecular mechanism. We examined the effects of daphnetin on splenocytes cultured in Th17 conditions, lung epithelial cells, and a mouse model of bleomycin (BLM)-induced pulmonary fibrosis. We identified that daphnetin inhibited IL-17A production in developing Th17 cells. We also found that daphnetin suppressed epithelial-to-mesenchymal transition (EMT) in TGF-β-treated BEAS2B cells through the regulation of AKT phosphorylation. In BLM-treated mice, the oral administration of daphnetin attenuated lung histopathology and improved lung mechanical functions. Our findings clearly demonstrated that daphnetin inhibited IL-17A and EMT both in vitro and in vivo, thereby protecting against BLM-induced pulmonary fibrosis. Taken together, these results suggest that daphnetin has potent therapeutic effects on lung fibrosis by modulating both Th17 differentiation and the TGF-β signaling pathway, and we thus expect daphnetin to be a drug candidate for the treatment of IPF.

Indexed as

BleomycinIdiopathic Pulmonary FibrosisAnimalsInterleukin-17MiceTransforming Growth Factor betaUmbelliferonesBleomycindaphnetinInterleukin-17Transforming Growth Factor betaUmbelliferonesdaphnetinidiopathic pulmonary fibrosisIL-17ATGF-βTh17

Identifiers

PMID38132116
PMCPMC10742308
OpenAlexW4389489039

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.