Evidence map›Paper›PMID 31780948›Full record

ArticleFrontiers in pharmacology2019

Cryptotanshinone Attenuates Airway Remodeling by Inhibiting Crosstalk Between Tumor Necrosis Factor-Like Weak Inducer of Apoptosis and Transforming Growth Factor Beta 1 Signaling Pathways in Asthma.

Chongyang Wang, Mingyu Zheng, Yunho Choi, Jingzhi Jiang, Li Li, Junfeng Li, Chang Xu, Zhemin Xian, Yan Li, Hongmei Piao and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 20 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

12 authors at 2 institutions in 2 countries.

Chongyang WangDepartment of Anatomy, Histology and Embryology, Medical College, Yanbian University, Yanji, China.
Mingyu ZhengJilin Key Laboratory of Anaphylactic Disease, Yanbian University, Yanji, China.
Yunho ChoiDepartment of Anatomy, Medical School, Institute for Medical Sciences, Chonbuk National University, Jeonju, South Korea.
Jingzhi JiangDepartment of Anatomy, Histology and Embryology, Medical College, Yanbian University, Yanji, China.
Li LiDepartment of Anatomy, Histology and Embryology, Medical College, Yanbian University, Yanji, China.
Junfeng LiDepartment of Anatomy, Histology and Embryology, Medical College, Yanbian University, Yanji, China.
Chang XuDepartment of Anatomy, Histology and Embryology, Medical College, Yanbian University, Yanji, China.
Zhemin XianJilin Key Laboratory of Anaphylactic Disease, Yanbian University, Yanji, China.
Yan LiJilin Key Laboratory of Anaphylactic Disease, Yanbian University, Yanji, China.
Hongmei PiaoJilin Key Laboratory of Anaphylactic Disease, Yanbian University, Yanji, China.
Liangchang LiDepartment of Anatomy, Histology and Embryology, Medical College, Yanbian University, Yanji, China.
Guanghai YanDepartment of Anatomy, Histology and Embryology, Medical College, Yanbian University, Yanji, China.
Yanbian University · CNJeonbuk National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The study is to investigate the effect of cryptotanshinone (CTS) on airway remodeling and the possible mechanism. Male BALB/c mice were pretreated with CTS or dexamethasone 30 min before nebulized inhalation of ovalbumin (OVA). CTS significantly inhibited OVA-induced increases of eosinophils and neutrophils infiltration of bronchoalveolar lavage fluids (BALFs), reduced airway resistance in asthmatic mice, decreased the accumulation of inflammatory cells, the hyperplasia of goblet cells and the deposition of collagen in asthmatic mice lung tissue, as well as markedly attenuated the leakage of inflammatory cells and the level of OVA-specific immunoglobulin E in BALFs. CTS also inhibited the expressions of alpha-smooth muscle actin, tumor necrosis factor-like weak inducer of apoptosis (TWEAK), Fn14, transforming growth factor (TGF)-β1, Smad4, and phosphorylation of Smad2/3 and STAT3 (Tyr705). In comparison to TWEAK inhibitor or TWEAK small interfering RNA (siRNA), which were used to inhibit TWEAK/STAT3 signaling pathways, CTS caused a similar effect as them on airway remodeling. Additionally, CTS also played a similar role as the TGF-β1 inhibitor or TGF-β1 siRNA in TGF-β1/STAT3 signaling pathways in airway remodeling. The anti-inflammatory effects of CTS against OVA-induced airway remodeling may be through inhibiting STAT3, which further suppresses TWEAK and TGF-β1 signaling cross talk in asthma. CTS may be a promising therapeutic reagent for asthma treatment.

Indexed as

airway remodelingcryptotanshinoneSTAT3transforming growth factor beta 1tumor necrosis factor-like weak inducer of apoptosis

Identifiers

PMID31780948
PMCPMC6859802
OpenAlexW2982230616

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.