Pathophysiological Basis for The Development of Diabetes Mellitus in Diabetic Neuropathy
Abstract
Diabetes mellitus (DM) is one of the foremost medical and social challenges of the 21st century, and diabetic neuropathy (DN) is one of its most common complications, occurring in 50–60% of patients with long-standing disease. The aim of this study is to systematize current data on the pathophysiological mechanisms of DN and to analyze the role of metabolic, vascular, oxidative, inflammatory, and trophic factors in nerve tissue damage. A systematic literature review (2014–2024) was conducted using international and Russian databases (PubMed, Scopus, Web of Science, RSCI, eLIBRARY.RU) with the following keywords: "diabetes mellitus," "diabetic neuropathy," "hyperglycemia," "polyol pathway," "advanced glycation end-products," "oxidative stress," "nerve growth factor," and their Russian equivalents. The pathogenesis of DN involves the activation of the polyol pathway, the accumulation of advanced glycation end products, mitochondrial and endothelial dysfunction, chronic inflammation, and a deficiency of neurotrophic factors, all of which lead to progressive nerve tissue damage. Understanding these mechanisms offers opportunities for early diagnosis, the development of biomarkers, and pathogenetically-based therapy. A comprehensive approach to treatment can slow the progression of this complication and improve patients' quality of life.