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Last update 08 May 2025

AGGF1

Last update 08 May 2025

Basic Info

Synonyms

AGGF1, Angiogenic factor VG5Q, Angiogenic factor with G patch and FHA domains 1

+ [9]

Introduction

Promotes angiogenesis and the proliferation of endothelial cells. Able to bind to endothelial cells and promote cell proliferation, suggesting that it may act in an autocrine fashion.

Drugs associated with AGGF1

US11504420

Patent Mining

Target

AGGF1

Mechanism-

Active Org.

NantOmics LLC

Originator Org.

NantOmics LLC

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

CN116059319

Patent Mining

Target

AGGF1

Mechanism-

Active Org.

Huazhong University of Science & Technology

Originator Org.

Huazhong University of Science & Technology

Active Indication

Cachexia [+3]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with AGGF1

100 Translational Medicine associated with AGGF1

0 Patents (Medical) associated with AGGF1

Literatures (Medical) associated with AGGF1

15 Mar 2025·The FASEB Journal

Angiogenic factor AGGF1 is a general splicing factor regulating angiogenesis and vascular development by alternative splicing of SRSF6

Article

Author: Zhang, Rui ; Han, Jinxiang ; Zhao, Yan ; Zhang, Jingwen ; Lv, Wenchao ; Xu, Chengqi ; Ning, Kang ; Li, Mian ; Wang, Qing K. ; Lyu, Dayin

AbstractAGGF1 encodes an angiogenic factor that causes vascular disease Klippel–Trenaunay syndrome when mutated. AGGF1 also acts at the top of the genetic regulatory hierarchy for mesodermal differentiation of hemangioblasts, multipotent stem cells for differentiation of blood cells and vascular cells. Alternative splicing (AS) is a post‐transcriptional process that generates multiple mature mRNAs from a single primary transcript (pre‐mRNA), producing protein diversity. Deregulation of AS leads to many human diseases. The physiological role and mechanism of AGGF1 in AS are not clear. Full‐length transcriptome sequencing of human pulmonary artery endothelial cells (HPAECs) with AGGF1 silencing revealed 63 121 genes, including 1144 new unannotated genes, and showed that AGGF1 is a general splicing factor regulating AS of 436 genes, including SRSF6 regulating AS of many target genes. AGGF1 promoted the skipping of exon 3 that produces the full‐length SRSF6 protein, an evolutionarily conserved AS event. Overexpression of full‐length SRSF6 reversed the reduced cell proliferation, migration, and capillary tube formation of HPAECs with AGGF1 silencing. Knockdown of SRSF6 and overexpression of the shorter, alternatively spliced isoform of SRSF6 both inhibited HPAEC proliferation, migration, and capillary tube formation, whereas opposite results were obtained for overexpression of full‐length SRSF6. Knockdown of srsf6 impaired development of ISVs in zebrafish, whereas overexpression of srsf6 enhanced vascular development and partially rescued impaired ISV development in zebrafish embryos with aggf1 knockdown. Overall, our findings reveal that AGGF1 is a general splicing factor, and that AGGF1‐mediated exon 3 skipping of SRSF6 pre‐mRNA is important for endothelial cell functions, angiogenesis, and vascular development.

01 Aug 2024·The Journal of Dermatology

Serum levels of AGGF1: Potential association with cutaneous and cardiopulmonary involvements in systemic sclerosis

Article

Author: Sumida, Hayakazu ; Sato, Shinichi ; Takahashi, Takuya ; Segawa, Yuichiro ; Terui, Hitoshi ; Takahashi, Takehiro ; Ikawa, Tetsuya ; Yoshizaki, Ayumi ; Takahashi, Toshiya ; Asano, Yoshihide

AbstractSystemic sclerosis (SSc) is an autoimmune disease characterized by vasculopathy, aberrant immune activation, and extensive tissue fibrosis of the skin and internal organs. Because of the complicated nature of its pathogenesis, the underlying mechanisms of SSc remain incompletely understood. Angiogenic factor with a G‐patch domain and a Forkhead‐associated domain 1 (AGGF1) is a critical factor in angiogenesis expressed on vascular endothelial cells, associated with inflammatory and fibrotic responses. To elucidate the possible implication of AGGF1 in SSc pathogenesis, we investigated the association between serum AGGF1 levels and clinical manifestations in SSc patients. We conducted a cross‐sectional analysis of AGGF1 levels in sera from 60 SSc patients and 19 healthy controls with enzyme‐linked immunosorbent assay. Serum AGGF1 levels in SSc patients were significantly higher than those in healthy individuals. In particular, diffuse cutaneous SSc patients with shorter disease duration had higher levels compared to those with longer disease duration and limited cutaneous SSc patients. Patients with higher serum AGGF1 levels had a higher incidence of digital ulcers, higher modified Rodnan Skin Scores (mRSS), elevated serum Krebs von den Lungen‐6 (KL‐6) levels, C‐reactive protein levels, and right ventricular systolic pressures (RVSP) on the echocardiogram, whereas they had reduced percentage of vital capacity (%VC) and percentage of diffusing capacity of the lungs for carbon monoxide (%DLCO) in pulmonary functional tests. In line, serum AGGF1 levels were significantly correlated with mRSS, serum KL‐6 and surfactant protein D levels, RVSP, and %DLCO. These results uncovered notable correlations between serum AGGF1 levels and key cutaneous and vascular involvements in SSc, suggesting potential roles of AGGF1 in SSc pathogenesis.

01 Jun 2024·Biochemical and Biophysical Research Communications

Diosgenin improves post-myocardial infarction cardiac function via HAND2-induced angiogenesis

Article

Author: Liu, Longfei ; Lu, Qiulun ; Liu, Xuehua ; Peng, Yuzhu ; Shen, Dehong

While diosgenin has been demonstrated effective in various cardiovascular diseases, its specific impact on treating heart attacks remains unclear. Our research revealed that diosgenin significantly improved cardiac function in a myocardial infarction (MI) mouse model, reducing cardiac fibrosis and cell apoptosis while promoting angiogenesis. Mechanistically, diosgenin upregulated the Hand2 expression, promoting the proliferation and migration of endothelial cells under hypoxic conditions. Acting as a transcription factor, HAND2 activated the angiogenesis-related gene Aggf1. Conversely, silencing Hand2 inhibited the diosgenin-induced migration of hypoxic endothelial cells and angiogenesis. In summary, these findings provide new insights into the protective role of diosgenin in MI, validating its effect on angiogenic activity and providing a theoretical basis for clinical treatment strategies.

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AGGF1

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