Diabetic foot syndrome is one of the most dangerous chronic diabetes complications. The well-established risk factors of impaired foot ulcers healing include continuing wound injury, impaired blood flow, hyperglycemia, infection joining. However, at the cellular and molecular levels, the pathogenesis of chronic ulcers in diabetes is much more complex and arcane process. Non-healing wounds are characterized by the acute inflammatory response deficiency, altered transition from the inflammatory to the proliferative phase, impaired proliferation and remodeling processes. Whereas the innate immunity role in the chronic foot ulcers pathogenesis has been studied well enough adaptive immunity role is known much worse. This review describes the stages and main wound healing mechanisms under normal conditions as well as their impairment on cellular and molecular levels in diabetes mellitus. To date, the question remains open about the significance of each of the mechanisms described and accordingly about the future research directions on the new preventive and therapeutic approaches development.