糖尿病性神経障害の発症メカニズム

Pathogenic Mechanisms of Diabetic Neuropathy

糖尿病性神経障害は末梢神経疾患の中で最も患者数が多く，また糖尿病の慢性合併症の中で最も早期かつ高頻度に出現する。末梢神経を構成するニューロン，シュワン細胞，血管内皮細胞などの代謝異常が本症の発症・増悪に深く関与することが報告されてきたが，いまだに不明な点も多く疾患修飾薬の開発は遅れている。本論では筆者らの研究を含め，神経障害の発症メカニズム解明および治療戦略に関する最近の知見を紹介する。

Abstract

Diabetes stands as the predominant cause of peripheral neuropathy, and diabetic neuropathy (DN) is an early-onset and most frequent complication of diabetes. Distal symmetric polyneuropathy is the major form of DN; however, various patterns of nerve injury can manifest. Growing evidence suggests that hyperglycemia-related metabolic disorders in neurons, Schwann cells, and vascular endothelial cells play a major role in the development and progression of DN; however, its pathogenesis and development of disease-modifying therapies warrant further investigation. Herein, recent studies regarding the possible pathogenic factors of DN (polyol and other collateral glycolysis pathways, glycation, oxidative stress, Rho/Rho kinase signaling pathways, etc.) and therapeutic strategies targeting these factors are introduced.