Seed germination is a critical developmental transition regulated by coordinated physiological and biochemical processes during the triphasic imbibition process. Water uptake is followed by membrane repair, restoration of mitochondrial respiration, ATP production and activation of hydrolytic enzymes involved in reserve mobilization. In this context, silver nanoparticle (AgNP) seed priming has emerged as a promising strategy to enhance germination by modulating early biochemical events through controlled redox signalling, although its effects vary among species and experimental conditions. This review integrates physiological, biochemical and molecular evidence to propose a seed-centred mechanistic framework explaining how AgNPs regulate germination through redox-dependent signalling networks. During imbibition, low AgNP concentrations can induce transient reactive oxygen species production through the combined effects of nanoparticles and released Ag⁺ ions, together with moderate thiol-based redox shifts acting as developmental signals. These signals activate antioxidant systems, mitogen-activated protein kinase cascades and hormone-dependent pathways coordinating metabolic activation and membrane repair. Controlled redox modulation may also establish a primed physiological state that improves tolerance to abiotic stress during early seedling establishment. In contrast, excessive AgNP or Ag⁺ exposure disrupts glutathione-based redox buffering, causing oxidative damage, mitochondrial dysfunction and inhibition of germination. The magnitude and direction of these responses depend on intrinsic seed traits, including seed coat permeability, imbibition kinetics and antioxidant capacity, as well as nanoparticle properties such as size, surface chemistry and ion release dynamics. Distinguishing nanoparticle-specific effects from Ag⁺-mediated toxicity is therefore essential for interpreting nanopriming outcomes and developing safe, species-specific crop applications.