Evidence map›Paper›PMID 30443024›Full record

ArticleScientific reports2018

A standardized herbal extract PM014 ameliorates pulmonary fibrosis by suppressing the TGF-β1 pathway.

Kyung Hwa Kim, Sujin Lee, Hyunji Lee, Dasom Shin, Daeun Min, Miran Kim, Byeol Ryu, Hyeon Woo Kim, Hyunsu Bae

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. 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
2.7field-weighted citation impact, top 9% 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, 27 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Loss of SP-A in the Lung Exacerbates Pulmonary Fibrosis.International journal of molecular sciences · 2022
    Article
  6. Article
  7. Review
  8. Article
  9. Article
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  11. Review
  12. Article
  13. Article
  14. Terrestrosin D fromPharmaceutical biology · 2019
    Article
  15. 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 3 institutions in 1 country.

Kyung Hwa KimDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, 02447, South Korea.
Sujin LeeDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, 02447, South Korea.
Hyunji LeeDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, 02447, South Korea.
Dasom ShinDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, 02447, South Korea.
Daeun MinDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, 02447, South Korea.
Miran KimCentral Research Institute, Hanlim Pharm. Co. Ltd., Yongin, 17040, South Korea.
Byeol RyuCollege of Pharmacy and Research Institute of Pharmaceutical Science, Seoul National University, Seoul, 08826, South Korea.
Hyeon Woo KimCollege of Pharmacy and Research Institute of Pharmaceutical Science, Seoul National University, Seoul, 08826, South Korea.
Hyunsu BaeDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, 02447, South Korea. hbae@khu.ac.kr.ORCID http://orcid.org/0000-0002-0299-3582
Kyung Hee University · KRSeoul National University · KRHanlim Pharm (South Korea) · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a devastating and common chronic lung disease pathologically characterized by loss of epithelial cells and activation of fibroblasts and myofibroblasts. The etiology of IPF remains unclear and the disease pathology is poorly understood with no known efficacious therapy. PM014 is an herbal extract that has been shown to have beneficial effects in pulmonary diseases, which are likely to exert anti-inflammatory bioactions. In the present study, we observed that bleomycin (BLM) caused increased inflammatory infiltration as well as collagen deposition in lungs of mice on day 14 after treatment. Administration of PM014 suppressed BLM-induced inflammatory responses and fibrotic changes in dose-dependent manner in mice. Additionally, we provided in vitro evidence suggesting that PM014 inhibited TGF-β1-induced epithelial-mesenchymal transition (EMT) and fibroblast activation in alveolar epithelial cells and human lung fibroblasts from healthy donor and IPF patients. PM014 appeared to target TGF-β1 signaling via Smad-dependent pathways and p38 mitogen-activated protein kinases (MAPKs) pathways. Taken together, our data suggest that PM014 administration exerts a protective effect against lung fibrosis and highlight PM014 as a viable treatment option that may bring benefits to patient with IPF.

Indexed as

Signal TransductionA549 CellsAnimalsAnti-Inflammatory AgentsBleomycinBody WeightCell MovementEpithelial CellsEpithelial-Mesenchymal TransitionFibroblastsHumansIdiopathic Pulmonary FibrosisMaleMice, Inbred C57BLp38 Mitogen-Activated Protein KinasesPlant ExtractsAnti-Inflammatory AgentsBleomycinp38 Mitogen-Activated Protein KinasesPlant ExtractsSmad ProteinsTransforming Growth Factor beta1

Identifiers

PMID30443024
PMCPMC6237877
OpenAlexW2899828813

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.