Canine influenza virus (CIV), an important lineage of influenza A virus (IAV) adapted to canine hosts, has emerged as a significant concern in zoonotic disease control. In recent years, CIV has exhibited distinct regional epidemic patterns worldwide, with H3N8 and H3N2 being the two predominant subtypes originating from cross-species transmission of equine and avian influenza viruses, respectively. This review systematically outlines the global epidemiological status of CIV and elaborates on the key molecular mechanisms underlying its interspecies barrier crossing and host adaptation. These adaptive mechanisms involve alterations in hemagglutinin receptor-binding specificity (e.g., the convergent W222L mutation), structural variations in the neuraminidase stalk region, adaptive mutations in the polymerase complex (e.g., PB2 I714S, E627K, D701N), immune antagonism by non-structural proteins (e.g., NS1-mediated suppression of the NLRP3 inflammasome), and genetic diversification through reassortment. Collectively, these evolutionary traits enhance viral replication efficiency, transmissibility, and immune evasion in mammalian hosts. A comprehensive understanding of the cross-species transmission patterns and adaptive evolution of CIV is crucial for developing effective prevention strategies and novel vaccines.