ITGA10 (integrin subunit alpha 10) functions as a collagen-binding receptor that mediates cell-matrix adhesion through integrin α10/β1 complex formation and activates PI3K/AKT signaling pathways 1. In developmental contexts, ITGA10 is highly expressed in proximal tubules during early kidney development (13 weeks gestation) and maintains expression postnatally, suggesting roles in both genitourinary tract development and kidney homeostasis maintenance 2. ITGA10 expression is dynamically regulated during osteoblast differentiation and is critical for osteogenic potential; the transcription factor Kaiso directly targets ITGA10 to promote osteoblast differentiation via PI3K/AKT signaling 3. In pathological contexts, ITGA10 plays significant roles in disease progression. ZIP10-mediated upregulation of ITGA10 drives osteosarcoma proliferation and chemoresistance through PI3K/AKT activation 1, while TET2-dependent epigenetic regulation of ITGA10 protects against sepsis-induced acute lung injury by preventing endothelial dysfunction 4. Low ITGA10 expression correlates with dental implant failure in type 2 diabetic patients, impairing bone marrow mesenchymal stem cell adhesion, migration, and osteogenic differentiation 5. ITGA10 is also upregulated in activated fibroblasts during vascular remodeling 6 and identified as a hub gene in aortic valve disease pathogenesis 7. These findings position ITGA10 as a critical integrin mediating cell-matrix interactions essential for skeletal development, bone homeostasis, and endothelial integrity.