Evidence map›Paper›PMID 35583801›Full record

ArticleHuman cell2022

The inhibitory effects of Dulaglutide on cellular senescence against high glucose in human retinal endothelial cells.

Shen Nian, Yajing Mi, Kai Ren, Shanwei Wang, Mingkai Li, Di Yang

Abstract read
PubMed Publisher
In one paragraph

Article in Human cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
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  8. Anti-Inflammatory Effects of GLP-1R Activation in the Retina.International journal of molecular sciences · 2022
    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

6 authors at 2 institutions in 1 country.

Shen NianDepartment of Pathology, Xi'an Medical University, No. 1, Xinwang Road, Weiyang District, Xi'an, 710021, Shaanxi, China. shennian@xiyi.edu.cn.ORCID http://orcid.org/0000-0003-1140-8135
Yajing MiInstitute of Basic Medicine Science, Xi'an Medical University, Xi'an, 710021, Shaanxi, China.
Kai RenDepartment of Biochemistry and Molecular Biology, Xi'an Medical University, Xi'an, 710021, Shaanxi, China.
Shanwei WangDepartment of Pathology, Xi'an Medical University, No. 1, Xinwang Road, Weiyang District, Xi'an, 710021, Shaanxi, China.
Mingkai LiSchool of Public Health, Xi'an Medical University, Xi'an, 710021, Shaanxi, China.
Di YangDepartment of Ophthalmology, First Affiliated Hospital of Kunming Medical University, Kunming Medical University, No. 295, Xichang Road, Kunming, 650032, Yunnan, China.
Xi'an Medical University · CNKunming Medical University · CN

Funding

National Natural Science Foundation of China 81860174National Natural Science Foundation of China 81873740Natural Science Basic Research Plan of Shaanxi Province 2020JM-612Yunnan Health Training Project of High Level Talents H-2019055
6 · The paper itself

Abstract

Diabetic nephropathy is one of the most important chronic microvascular complications of diabetes, and its main feature is diabetic glomerulosclerosis. Endothelial sirtuin 1 (SIRT1) expression is related to aging, and reducing SIRT1 expression promotes endothelial cell aging. Plasminogen activator inhibitor-1 (PAI-1) can be synthesized in a variety of cells, such as endothelial cells. Dulaglutide is a glucagon-like peptide-1 (GLP-1) drug, and it can activate the GLP-1 receptor and promote the conversion of intracellular adenosine triphosphate to adenylate cyclase, thereby activating phosphokinase A, and regulating blood glucose levels effectively in the body. We analyzed the effects of Dulaglutide on inhibiting cell senescence by studying the effects of its different concentrations on telomerase activity and senescence-related gene expression. Our results suggest that Dulaglutide can alleviate high-glucose-induced oxidative stress in human retinal endothelial cells by restoring the expressions of SIRT1 and endothelial nitric oxide synthase (eNOS), thereby inhibiting the expression of PAI-1, and restoring telomerase activity. This suggests that the activity of retinal endothelial cells can be controlled by regulating the expression of SIRT1, so as to achieve the effect of treating diabetic retinopathy.

Indexed as

Endothelial CellsTelomeraseCells, CulturedCellular SenescenceGlucagon-Like PeptidesGlucoseHumansImmunoglobulin Fc FragmentsPlasminogen Activator Inhibitor 1Recombinant Fusion ProteinsSirtuin 1dulaglutideGlucagon-Like PeptidesGlucoseImmunoglobulin Fc FragmentsPlasminogen Activator Inhibitor 1Recombinant Fusion ProteinsSirtuin 1TelomeraseCellular senescenceDiabetesDulaglutideHigh glucoseRetinal endothelial cells

Identifiers

PMID35583801
OpenAlexW4280524154

What Socratic holds

Textmetadata
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 Socratic graph.