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Flavonoid-Mediated Suppression of Tumor Angiogenesis: Roles of Ang-Tie/PI3K/AKT
- Source :
- Pathophysiology, Vol 31, Iss 4, Pp 596-607 (2024)
- Publication Year :
- 2024
- Publisher :
- MDPI AG, 2024.
-
Abstract
- Angiogenesis is a process involved in the formation of new blood capillaries from pre-existing ones. It is regulated by several anti-angiogenic molecules involved in tumor growth and metastasis. The endothelial angiopoietin Ang-Tie/PI3K/AKT growth receptor pathway is necessary for healthy vascular development. The activation of AKT is controlled by a multistep process involving phosphoinositide 3-kinase (PI3K). This article aims to provide an overview of the role and mechanism of the Ang-Tie/PI3K/AKT signaling pathways and the potential of flavonoids as anti-angiogenic drugs. Flavonoids have shown great potential in preventing angiogenesis by targeting signaling pathways and exhibit additional anti-cancer properties. Research studies have revealed that the currently available anti-angiogenic drugs do not meet the safety and efficacy standards for treating tumor growth. Phytocompounds have long been a valuable resource for the development of novel therapeutic drugs. This article explores recent findings explaining the role and mechanism of the Ang-Tie/PI3K/AKT signaling pathways, as well as the interaction of flavonoids with angiogenic signaling pathways as a novel therapeutic approach. Several investigations have shown that synergistic studies of natural phytocompounds have great potential to target these pathways to inhibit tumor growth. Therefore, flavonoid-based medications may offer a more effective synergistic strategy to treat cancer.
- Subjects :
- angiogenesis
anti-cancerous
flavonoid
metabolism
tumor
phytocompound
Physiology
QP1-981
Subjects
Details
- Language :
- English
- ISSN :
- 1873149X
- Volume :
- 31
- Issue :
- 4
- Database :
- Directory of Open Access Journals
- Journal :
- Pathophysiology
- Publication Type :
- Academic Journal
- Accession number :
- edsdoj.910c6ce6c5614e1b90e3c0d3cba525d6
- Document Type :
- article
- Full Text :
- https://doi.org/10.3390/pathophysiology31040043