Evidence map›Paper›PMID 31412804›Full record

ArticleBMC nephrology2019

Uric acid regulates NLRP3/IL-1β signaling pathway and further induces vascular endothelial cells injury in early CKD through ROS activation and K

Wei Yin, Qiao-Ling Zhou, Sha-Xi OuYang, Ying Chen, Yu-Ting Gong, Yu-Mei Liang

Open access · goldAbstract read
In one paragraph

Article in BMC nephrology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 84 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

6 authors at 3 institutions in 1 country.

Wei YinDepartment of Nephrology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, No.61, West Jiefang Road, Changsha, 410005, Hunan Province, People's Republic of China.
Qiao-Ling ZhouDepartment of Nephrology, Xiangya Hospital, Central South University, Changsha, 410008, People's Republic of China.
Sha-Xi OuYangDepartment of Nephrology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, No.61, West Jiefang Road, Changsha, 410005, Hunan Province, People's Republic of China.
Ying ChenDepartment of Nephrology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, No.61, West Jiefang Road, Changsha, 410005, Hunan Province, People's Republic of China.
Yu-Ting GongDepartment of Nephrology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, No.61, West Jiefang Road, Changsha, 410005, Hunan Province, People's Republic of China.
Yu-Mei LiangDepartment of Nephrology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, No.61, West Jiefang Road, Changsha, 410005, Hunan Province, People's Republic of China. liangyumei452@163.com.
Hunan Normal University · CNHunan Provincial People's Hospital · CNXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic kidney disease (CKD) has been considered as a major health problem in the world. Increasing uric acid (UA) could induce vascular endothelial injury, which is closely related to microinflammation, oxidative stress, and disorders of lipids metabolism. However, the specific mechanism that UA induces vascular endothelial cells injury in early CKD remains unknown.

methodsHuman umbilical vein endothelial cells (HUVECs) were cultured and subjected to different concentrations of UA for different periods. Early CKD rat model with elevated serum UA was established. Western blotting and quantitative real-time PCR (qPCR) were applied for measuring protein and mRNA expression of different cytokines. The animals were sacrificed and blood samples were collected for measurement of creatinine, UA, IL-1β, TNF-α, and ICAM-1. Renal tissues were pathologically examined by periodic acid-Schiff (PAS) or hematoxylin-eosin (HE) staining.

resultsThe expression of IL-1β, ICAM-1, NLRP3 complexes, and activation of NLRP3 inflammasome could be induced by UA, but the changes induced by UA were partially reversed by siRNA NLRP3 or caspase 1 inhibitor. Furthermore, we identified that UA regulated the activation of NLRP3 inflammasome by activating ROS and K

conclusionsUA could regulate NLRP3/IL-1β signaling pathway through ROS activation and K

Indexed as

AnimalsCreatinineDisease Models, AnimalEndothelium, VascularHumansHuman Umbilical Vein Endothelial CellsInflammasomesIntercellular Adhesion Molecule-1Interleukin-1betaMaleNLR Family, Pyrin Domain-Containing 3 ProteinPotassiumRatsRats, Sprague-DawleyReactive Oxygen SpeciesRenal Insufficiency, ChronicCreatinineInflammasomesIntercellular Adhesion Molecule-1Interleukin-1betainterleukin-1beta-converting enzyme inhibitorNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratPotassiumReactive Oxygen SpeciesRNA, Small InterferingSerpinsTumor Necrosis Factor-alphaUric AcidViral ProteinsEarly CKDK+ effluxNLRP3/IL-1βROS activationUric acid

Identifiers

PMID31412804
PMCPMC6694569
OpenAlexW2968906039

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.