Evidence map›Paper›PMID 38491522›Full record

ArticleCell communication and signaling : CCS2024

Endothelial β-catenin upregulation and Y142 phosphorylation drive diabetic angiogenesis via upregulating KDR/HDAC9.

Zhenfeng Chen, Bingqi Lin, Xiaodan Yao, Jie Weng, Jinlian Liu, Qi He, Ke Song, Chuyu Zhou, Zirui Zuo, Xiaoxia Huang and 4 more

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

Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

7 citing papers in PubMed, 6 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

14 authors at 1 institution in 1 country.

Zhenfeng Chen *Guangdong Provincial Key Laboratory of Cardiac Function and Microcirculation, Department of Pathophysiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Bingqi Lin *Guangdong Provincial Key Laboratory of Cardiac Function and Microcirculation, Department of Pathophysiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Xiaodan YaoGuangdong Provincial Key Laboratory of Cardiac Function and Microcirculation, Department of Pathophysiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Jie WengGuangdong Provincial Key Laboratory of Cardiac Function and Microcirculation, Department of Pathophysiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Jinlian LiuGuangdong Provincial Key Laboratory of Cardiac Function and Microcirculation, Department of Pathophysiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Qi HeGuangdong Provincial Key Laboratory of Cardiac Function and Microcirculation, Department of Pathophysiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Ke SongGuangdong Provincial Key Laboratory of Cardiac Function and Microcirculation, Department of Pathophysiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Chuyu ZhouGuangdong Provincial Key Laboratory of Cardiac Function and Microcirculation, Department of Pathophysiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Zirui ZuoGuangdong Provincial Key Laboratory of Cardiac Function and Microcirculation, Department of Pathophysiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Xiaoxia HuangGuangdong Provincial Key Laboratory of Cardiac Function and Microcirculation, Department of Pathophysiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Zhuanhua LiuGuangdong Provincial Key Laboratory of Cardiac Function and Microcirculation, Department of Pathophysiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Qiaobing HuangGuangdong Provincial Key Laboratory of Cardiac Function and Microcirculation, Department of Pathophysiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Qiulin XuDepartment of Intensive Care Unit, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Science, Southern Medical University, Guangzhou, 510515, China. xuqiulin@gdph.org.cn.
Xiaohua GuoGuangdong Provincial Key Laboratory of Cardiac Function and Microcirculation, Department of Pathophysiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China. lanblue@smu.edu.cn.
Southern Medical University · CN

Funding

College Students' Innovative Entrepreneurial Training Plan Program 202212121015National Natural Science Foundation of China 31871183
6 · The paper itself

Abstract

backgroundDiabetic angiogenesis is closely associated with disabilities and death caused by diabetic microvascular complications. Advanced glycation end products (AGEs) are abnormally accumulated in diabetic patients and are a key pathogenic factor for diabetic angiogenesis. The present study focuses on understanding the mechanisms underlying diabetic angiogenesis and identifying therapeutic targets based on these mechanisms.

methodsIn this study, AGE-induced angiogenesis serves as a model to investigate the mechanisms underlying diabetic angiogensis. Mouse aortic rings, matrigel plugs, and HUVECs or 293T cells were employed as research objects to explore this pathological process by using transcriptomics, gene promoter reporter assays, virtual screening and so on.

resultsHere, we found that AGEs activated Wnt/β-catenin signaling pathway and enhanced the β-catenin protein level by affecting the expression of β-catenin degradation-related genes, such as FZDs (Frizzled receptors), LRPs (LDL Receptor Related Proteins), and AXIN1. AGEs could also mediate β-catenin Y142 phosphorylation through VEGFR1 isoform5. These dual effects of AGEs elevated the nuclear translocation of β-catenin and sequentially induced the expression of KDR (Kinase Insert Domain Receptor) and HDAC9 (Histone Deacetylase 9) by POU5F1 and NANOG, respectively, thus mediating angiogenesis. Finally, through virtual screening, Bioymifi, an inhibitor that blocks VEGFR1 isoform5-β-catenin complex interaction and alleviates AGE-induced angiogenesis, was identified.

conclusionCollectively, this study offers insight into the pathophysiological functions of β-catenin in diabetic angiogenesis.

Indexed as

Diabetes ComplicationsDiabetes MellitusAngiogenesisAnimalsbeta CateninHistone DeacetylasesHumansMicePhosphorylationRepressor ProteinsUp-RegulationVascular Endothelial Growth Factor Receptor-2Wnt Signaling Pathwaybeta CateninCTNNB1 protein, humanCTNNB1 protein, mouseHDAC9 protein, humanHdac9 protein, mouseHistone DeacetylasesKDR protein, humanKdr protein, mouseRepressor ProteinsVascular Endothelial Growth Factor Receptor-2Advanced glycation end productsBioymifiDiabetic angiogenesisHDAC9KDRPhosphorylationVEGFR1 isoform5β-catenin

Identifiers

PMID38491522
PMCPMC10941375
OpenAlexW4392849919

What Socratic holds

Textmetadata
LicenceCC BY
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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.