AGGF1, the angiogenic factor with G-patch and FHA domain 1, is a crucial gene involved in multiple biological processes. It is an angiogenic factor that regulates cell differentiation, proliferation, migration, apoptosis, autophagy and endoplasmic reticulum stress. It also promotes vasculogenesis and angiogenesis, and is associated with pathways like TGF-β1 maturation, ERK1/2 signaling, NF-κB signaling, and mTOR-S6K-ERK1/2 signaling. Its dysregulation is related to various diseases, highlighting its overall biological importance. Genetic models, such as knockout mouse models, are valuable for studying its functions [1-3, 6, 9, 10].

In thoracic aortic aneurysm (TAA) studies, Aggf1 expression is reduced in affected tissues. Aggf1+/- mice and VSMC-specific Aggf1smcKO knockout mice show aggravated TAA phenotypes. Mechanistically, AGGF1 enhances the interaction between integrin α7 and LAP-TGF-β1, blocking the formation of mature TGF-β1 and inhibiting Smad2/3 and ERK1/2 phosphorylation in VSMCs [1].

In skeletal muscle atrophy, heterozygous Aggf1+/- mice have exacerbated atrophy phenotypes. AGGF1 interacts with TWEAK, reducing TWEAK-Fn14 interaction, inhibiting NF-κB p65 phosphorylation, MuRF1 expression, and enhancing autophagy to attenuate atrophy [2].

In zebra fish, knockout of aggf1 impairs the specification of hemangioblasts and HSPCs, hematopoiesis, and vascular development, uncovering a novel Aggf1-mTOR-S6K-ERK1/2 signaling axis [3].

In placenta accreta spectrum, decreased AGGF1 promotes trophoblast over-invasion by mediating the P53 signaling pathway under miR-1296-5p regulation [4].

In conclusion, AGGF1 plays essential roles in angiogenesis, cell regulation, and tissue homeostasis. Model-based research, especially using Aggf1 KO/CKO mouse models, has revealed its significance in diseases like TAA, skeletal muscle atrophy, and placenta accreta spectrum. Understanding AGGF1 provides insights into disease mechanisms and potential therapeutic strategies for these conditions.