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Fracture healing is a complex biological process influenced by systemic conditions and medications. Given the high prevalence of cardiovascular disease in fracture surgery patients and the use of beta-blockers, evidence linking beta-adrenergic signaling to bone metabolism has raised interest in their effects on postoperative healing. This narrative review synthesizes experimental, translational, and clinical evidence regarding the impact of beta-blocker therapy on fracture healing. A structured literature-based approach was used to evaluate studies addressing β-adrenergic signaling in cardiovascular regulation, bone cell function, angiogenesis, and postoperative fracture outcomes. Both preclinical models and observational human studies were critically analyzed to identify mechanistic pathways and clinical associations. Experimental studies indicate that β-adrenergic signaling inhibits osteoblast activity and callus formation, enhances osteoclast activity, and impairs angiogenesis during bone repair. Beta-blockade, particularly with non-selective and lipophilic agents, may counteract these effects, thereby promoting bone formation and microvascular function in animal models. However, clinical evidence remains heterogeneous. Some observational studies report potential benefits, including reduced postoperative mortality or lower fracture risk, whereas other studies show no significant association with healing outcomes or suggest a possible increase in non-union risk. Confounding factors such as comorbid cardiovascular disease, polypharmacy, and differences in drug selectivity limit causal interpretation. Beta-blocker therapy may influence fracture healing through neurovascular and cellular pathways, but current clinical evidence is insufficient to confirm a definitive beneficial or harmful effect. Further prospective, mechanistic, and stratified clinical studies are required to clarify their role in optimizing both cardiovascular and skeletal outcomes in patients undergoing fracture surgery.