Evidence map›Paper›PMID 38652215›Full record

ReviewMolecular and cellular biochemistry2025

Ang-1 and VEGF: central regulators of angiogenesis.

Yuanqin Zhao, Bo Yu, Yanxia Wang, Shiming Tan, Qian Xu, Zhaoyue Wang, Kun Zhou, Huiting Liu, Zhong Ren, Zhisheng Jiang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 2026
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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 1 institution in 1 country.

Yuanqin ZhaoKey Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, China.
Bo YuKey Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, China.
Yanxia WangKey Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, China.
Shiming TanKey Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, China.
Qian XuKey Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, China.
Zhaoyue WangKey Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, China.
Kun ZhouKey Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, China.
Huiting LiuKey Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, China.
Zhong RenKey Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, China.
Zhisheng JiangKey Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, China. zsjiang2017@163.com.
University of South China · CN

Funding

"Double First-Class"project for innovative Group of Basic Medicine, Universityof South China, and Scientific Research Fund of Hunan Provincial Education Department 20C1576International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province 2018WK4031Special Funding for Construction of Innovative Provinces in Hunan Province 2020SK2105the National Kev Research and Development Program of China 2019YFA0801601the National Natural Science Foundation of China 9183910381670429
6 · The paper itself

Abstract

Angiopoietin-1 (Ang-1) and Vascular Endothelial Growth Factor (VEGF) are central regulators of angiogenesis and are often inactivated in various cardiovascular diseases. VEGF forms complexes with ETS transcription factor family and exerts its action by downregulating multiple genes. Among the target genes of the VEGF-ETS complex, there are a significant number encoding key angiogenic regulators. Phosphorylation of the VEGF-ETS complex releases transcriptional repression on these angiogenic regulators, thereby promoting their expression. Ang-1 interacts with TEK, and this phosphorylation release can be modulated by the Ang-1-TEK signaling pathway. The Ang-1-TEK pathway participates in the transcriptional activation of VEGF genes. In summary, these elements constitute the Ang-1-TEK-VEGF signaling pathway. Additionally, Ang-1 is activated under hypoxic and inflammatory conditions, leading to an upregulation in the expression of TEK. Elevated TEK levels result in the formation of the VEGF-ETS complex, which, in turn, downregulates the expression of numerous angiogenic genes. Hence, the Ang-1-dependent transcriptional repression is indirect. Reduced expression of many target genes can lead to aberrant angiogenesis. A significant overlap exists between the target genes regulated by Ang-1-TEK-VEGF and those under the control of the Ang-1-TEK-TSP-1 signaling pathway. Mechanistically, this can be explained by the replacement of the VEGF-ETS complex with the TSP-1 transcriptional repression complex at the ETS sites on target gene promoters. Furthermore, VEGF possesses non-classical functions unrelated to ETS and DNA binding. Its supportive role in TSP-1 formation may be exerted through the VEGF-CRL5-VHL-HIF-1α-VH032-TGF-β-TSP-1 axis. This review assesses the regulatory mechanisms of the Ang-1-TEK-VEGF signaling pathway and explores its significant overlap with the Ang-1-TEK-TSP-1 signaling pathway.

Indexed as

Angiopoietin-1Gene Expression RegulationNeovascularization, PathologicNeovascularization, PhysiologicSignal TransductionVascular Endothelial Growth Factor AAngiogenesisAnimalsHumansReceptors, TIEReceptor, TIE-2Angiopoietin-1ANGPT1 protein, humanReceptors, TIEReceptor, TIE-2TEK protein, humanVascular Endothelial Growth Factor AVEGFA protein, humanAng-1AngiogenesisTEKTSP-1VEGF

Identifiers

PMID38652215
OpenAlexW4395038896

What OpenQuestion 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 OpenQuestion graph.