Evidence map›Paper›PMID 31216990›Full record

ArticleBMC molecular and cell biology2019

SAA1 increases NOX4/ROS production to promote LPS-induced inflammation in vascular smooth muscle cells through activating p38MAPK/NF-κB pathway.

Mei-Hong Yu, Xi Li, Qian Li, Shi-Jing Mo, Yin Ni, Fang Han, Yi-Bin Wang, Yue-Xing Tu

Open access · goldAbstract read
In one paragraph

Article in BMC molecular and cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

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  9. Anti-inflammatory therapy of atherosclerosis: focusing on IKKβ.Journal of inflammation (London, England) · 2023
    Review
  10. Gut Molecules in Cardiometabolic Diseases: The Mechanisms behind the Story.International journal of molecular sciences · 2023
    Review
  11. Article
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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 3 institutions in 1 country.

Mei-Hong YuDepartment of ICU, Chunan First People's Hospital, Hangzhou, 311700, China.
Xi LiCentre of Laboratory Medicine, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, 310014, China.
Qian LiDepartment of ICU, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, 310014, China.
Shi-Jing MoDepartment of ICU, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, 310014, China.
Yin NiDepartment of ICU, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, 310014, China.
Fang HanDepartment of ICU, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, 310014, China.
Yi-Bin WangDepartment of Cardiology, Chunan First People's Hospital, Hangzhou, 311700, China.
Yue-Xing TuDepartment of ICU, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, 310014, China. tuyuexing223@outlook.com.
Hangzhou Medical College · CNHangzhou First People's Hospital · CNZhejiang Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTo investigate the effects of serum amyloid A1 (SAA1) on lipopolysaccharide (LPS) -induced inflammation in vascular smooth muscle cells (VSMCs). SAA1 expression was detected in LPS induced VSMCs at different concentrations for different time by using Western blotting. After pre-incubation with recombinant SAA1 protein, VSMCs were treated with 1 μg/ml LPS for 24 h. The VSMCs were then divided into Control, SAA1 siRNA, Nox4 siRNA, LPS, LPS + SAA1 siRNA, LPS + Nox4 siRNA and LPS + SAA1 siRNA + Nox4 groups. MTT was performed to observe the toxicity of VSMCs. Lucigenin-enhanced chemiluminescence method was used to detect superoxide anion (O

resultsLPS promoted SAA1 protein expression in a concentration-/time-dependent manner. Recombinant SAA1 protein could increase NOX4/ROS production and promote the release of inflammatory factors (IL-1β, IL-6, IL-8, IL-17, TNF-α and MCP-1) in LPS (1 μg/ml) - induced VSMCs. Besides, both SAA1 siRNA and NOX-4 siRNA could not only enhance the O

conclusionSAA1-mediated NOX4/ROS pathway could activate p38MAPK/NF-κB pathway, thereby contributing to the release of inflammatory factors in LPS-induced VSMCs.

Indexed as

AnimalsCells, CulturedCell SurvivalCytokinesInflammationLipopolysaccharidesMaleMuscle, Smooth, VascularMyocytes, Smooth MuscleNADPH Oxidase 4NADPH OxidasesNF-kappa Bp38 Mitogen-Activated Protein KinasesRatsRats, Sprague-DawleyReactive Oxygen SpeciesCytokinesLipopolysaccharidesNADPH Oxidase 4NADPH OxidasesNF-kappa BNox4 protein, ratp38 Mitogen-Activated Protein KinasesReactive Oxygen SpeciesRecombinant ProteinsRNA, Small InterferingSerum Amyloid A ProteinInflammationLPSNOX-4/ROSp38MAPK/NF-κBSerum amyloid A1Vascular smooth muscle cell

Identifiers

PMID31216990
PMCPMC6582534
OpenAlexW2949828639

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.