Evidence map›Paper›PMID 29209448›Full record

ArticleOxidative medicine and cellular longevity2017

Sirt1 Protects Endothelial Cells against LPS-Induced Barrier Dysfunction.

Weijin Zhang, Yaoyuan Zhang, Xiaohua Guo, Zhenhua Zeng, Jie Wu, Yanan Liu, Jing He, Ruiting Wang, Qiaobing Huang, Zhongqing Chen

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
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  14. Histone Modifications in Acute Kidney Injury.Kidney diseases (Basel, Switzerland) · 2022
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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

10 authors at 2 institutions in 1 country.

Weijin ZhangDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.ORCID 0000-0002-1477-7465
Yaoyuan ZhangDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.ORCID 0000-0001-5837-8792
Xiaohua GuoGuangdong Key Lab of Shock and Microcirculation Research, Department of Pathophysiology, Southern Medical University, Guangzhou 510515, China.
Zhenhua ZengDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.ORCID 0000-0002-9509-1536
Jie WuDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.ORCID 0000-0002-7590-4368
Yanan LiuDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Jing HeDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Ruiting WangDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Qiaobing HuangGuangdong Key Lab of Shock and Microcirculation Research, Department of Pathophysiology, Southern Medical University, Guangzhou 510515, China.ORCID 0000-0001-8931-7378
Zhongqing ChenDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.ORCID 0000-0003-2482-949X
Nanfang Hospital · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis is a threatening health problem and characterized by microvascular dysfunction. In this study, we verified that LPS caused the downregulation of Sirt1 and the hyperpermeability of endothelial cells. Inhibition of Sirt1 with ex527 or Sirt1 siRNA displayed a higher permeability, while activation of Sirt1 with SRT1720 reversed the LPS-induced hyperpermeability, formation of fiber stress, and disruption of VE-cadherin distribution. In pulmonary microvascular vein endothelial cells isolated from wild-type mice, Sirt1 was attenuated upon LPS, while Sirt1 was preserved in a receptor of advanced glycation end product-knockout mice. The RAGE antibody could also diminish the downregulation and ubiquitination of Sirt1 in LPS-exposed human umbilical vein endothelial cells. An LPS-induced decrease in Sirt1 activity was attenuated by the RAGE antibody and TLR4 inhibitor.

Indexed as

Animalsbeta CateninDown-RegulationHeterocyclic Compounds, 4 or More RingsHumansHuman Umbilical Vein Endothelial CellsLipopolysaccharidesMiceMice, Inbred C57BLMice, KnockoutNADPH Oxidase 4PermeabilityReactive Oxygen SpeciesReceptor for Advanced Glycation End ProductsRNA InterferenceRNA, Small InterferingAger protein, mousebeta CateninHeterocyclic Compounds, 4 or More RingsLipopolysaccharidesNADPH Oxidase 4Reactive Oxygen SpeciesReceptor for Advanced Glycation End ProductsRNA, Small InterferingSirtuin 1SRT1720Superoxide DismutaseToll-Like Receptor 4Tumor Suppressor Protein p53

Identifiers

PMID29209448
PMCPMC5676476
OpenAlexW2765704810

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.