Evidence map›Paper›PMID 36613617›Full record

ArticleInternational journal of molecular sciences2022

Hydroxysafflower Yellow A Inhibits Vascular Adventitial Fibroblast Migration via NLRP3 Inflammasome Inhibition through Autophagy Activation.

Lin Liu, Qingzhuo Cui, Junna Song, Yang Yang, Yixin Zhang, Jiapeng Qi, Jingshan Zhao

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
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

7 authors at 1 institution in 1 country.

Lin LiuCollege of Pharmacy, Hebei University of Chinese Medicine, Shijiazhuang 050200, China.
Qingzhuo CuiCollege of Pharmacy, Hebei University of Chinese Medicine, Shijiazhuang 050200, China.
Junna SongCollege of Pharmacy, Hebei University of Chinese Medicine, Shijiazhuang 050200, China.
Yang YangDepartment of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei University of Chinese Medicine, Shijiazhuang 050200, China.
Yixin ZhangCollege of Pharmacy, Hebei University of Chinese Medicine, Shijiazhuang 050200, China.
Jiapeng QiDepartment of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei University of Chinese Medicine, Shijiazhuang 050200, China.
Jingshan ZhaoCollege of Pharmacy, Hebei University of Chinese Medicine, Shijiazhuang 050200, China.
Hebei University of Chinese Medicine · CN

Funding

Key program of Scientific and technological Research projects of Colleges and universities in Hebei Province ZD2017056Key Research and Development Project of Hebei Province 223777149DKey scientific Research Program of Hebei Provincial Department of Health 20170856Natural Science Foundation of Hebei Province H2020423061Science and technology innovation ability cultivation special projec of Hebei Province College and Middle School Students 22E50140DScience and Technology Project of Hebei Education Department QN2022092Scientific research Program of Hebei Administration of Traditional Chinese Medicine 2017009Scientific research Program of Hebei Administration of Traditional Chinese Medicine 2022080
6 · The paper itself

Abstract

Inflammation is closely associated with progression of vascular remodeling. The NLRP3 inflammasome is the key molecule that promotes vascular remodeling via activation of vascular adventitia fibroblast (VAF) proliferation and differentiation. VAFs have a vital effect on vascular remodeling that could be improved using hydroxysafflower yellow A (HSYA). However, whether HSYA ameliorates vascular remodeling through inhibition of NLRP3 inflammasome activation has not been explored in detail. Here, we cultured primary VAFs and analyzed the migration of VAFs induced by angiotensin II (ANG II) to determine the potential effects and mechanism of HSYA on VAF migration. The results thereof showed that HSYA remarkably inhibited ANG II-induced VAF migration, NLRP3 inflammasome activation, and the TLR4/NF-κB signaling pathway in a dose-dependent manner. In addition, it is worth noting that LPS promoted ANG II-induced VAF migration and NLRP3 inflammasome assembly, which could be significantly reversed using HSYA. Moreover, HSYA could be used to inhibit NLRP3 inflammasome activation by promoting autophagy. In conclusion, HSYA could inhibit ANG II-induced VAF migration through autophagy activation and inhibition of NLRP3 inflammasome activation through the TLR4/NF-κB signaling pathway.

Indexed as

AdventitiaInflammasomesAngiotensin IIAutophagyFibroblastsHumansNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinToll-Like Receptor 4Vascular RemodelingAngiotensin IIInflammasomesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinToll-Like Receptor 4autophagyhydroxysafflower yellow ANLRP3 inflammasomevascular adventitial fibroblasts

Identifiers

PMID36613617
PMCPMC9820330
OpenAlexW4312188071

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.