Arfgap3, also known as ADP ribosylation factor GTPase-activating protein 3, is a member of ArfGAPs. It is crucial for regulating vesicular trafficking pathways, especially in COPI coat assembly [1,2,4,5,6]. It is involved in intracellular protein transportation and has been linked to important biological processes such as muscle repair, cell proliferation, and autophagy [1,2]. Genetic models, like mouse models, have been instrumental in studying its functions.

In skeletal muscle, Arfgap3 is expressed during the repair process after injury and myoblast differentiation. Knockdown of Arfgap3 in C2C12 myoblasts blocks intracellular vesicle transport and glucose uptake, impairs myoblast proliferation, increases apoptosis, and hinders myotube differentiation [1]. In ageing skeletal muscle, its expression is downregulated. Knockdown of Arfgap3 in an ageing C2C12 model exacerbates impaired differentiation potential and mitochondrial dysfunction, while overexpression mitigates these effects. Arfgap3 also promotes autophagy through Rab5a-mediated signals in ageing skeletal muscle [2]. In prostate cancer cells, Arfgap3 is induced by dihydrotestosterone. Overexpression promotes cell proliferation and migration, and knockdown reduces LNCaP cell growth [3].

In conclusion, Arfgap3 is essential for regulating vesicle transport and has far-reaching effects on biological processes. Its role in muscle repair, ageing-related muscle decline, and cancer cell proliferation, as revealed by model-based research, highlights its importance in these disease areas. Understanding Arfgap3 provides potential therapeutic targets for skeletal muscle-related disorders and prostate cancer.