Itgav, also known as integrin alpha V, is a crucial gene encoding the integrin alpha V subunit. Integrin heterodimers containing this subunit are essential for development and play key roles in cell adhesion and signaling, involving pathways like TGF-β-dependent signaling [2]. Itgav is significant in various biological processes and diseases.

In liver fibrosis, knockdown of Runx2, which can bind to the Itgav promoter to promote its expression, alleviated fibrosis in mouse models, suggesting Itgav's role in HSC activation and fibrosis progression [1]. Conditional knockout of Itgav in myofibroblasts significantly attenuated radiation-induced lung fibrosis in mice by inhibiting αv integrin-mediated TGFβ1 activation [6]. In metastatic breast cancer, silencing of Itgav inhibited cell proliferation, invasion, and self-renewal [3]. In cutaneous carcinoma, ITGAV is a prognostic biomarker of relapse, and its knockdown in epithelial plastic cancer cells blocked epithelial-mesenchymal plasticity [4]. In head and neck squamous cell carcinoma, knockdown of ITGAV inhibited cell migration, invasion, viability, and colony formation [5].

In conclusion, Itgav is vital for cell adhesion and signaling. Gene knockout and knockdown studies in various mouse models have revealed its role in diseases such as liver fibrosis, radiation-induced lung fibrosis, metastatic breast cancer, cutaneous carcinoma, and head and neck squamous cell carcinoma. These findings provide potential therapeutic targets for these diseases.