Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra, Azinhaga de Santa Comba, 3004-548, Coimbra, Portugal.
CNC.IBILI Consortium, University of Coimbra, 3004-517, Coimbra, Portugal.
Mol Neurobiol. 2019 Mar;56(3):2202-2210. doi: 10.1007/s12035-018-1227-1. Epub 2018 Jul 12.
Diabetes mellitus is a chronic disease with numerous complications that severely impact on the quality of life of patients. Different neuropathies may arise as complications associated with the nervous system, both peripherally and at the central level. The mechanisms behind these neuronal complications are far from being clarified, but axonal transport impairment, a vital process for neuronal physiology, has been described in the context of experimental diabetes. Alterations in neuronal cytoskeleton and motor proteins, deficits in ATP supply or neuroinflammation, as processes that disturb the effective transport of cargoes along the axon, were reported as putative causes of axonal impairment, ultimately leading to axonal degeneration. The main goal of the present review is to reunite the main studies in the literature exploring diabetes-induced alterations likely involved in axonal transport deficits, and call the attention for the uttermost importance of further exploring the field. Understanding the mechanisms underlying neuronal deficits in diabetes is crucial for the development of new therapeutic strategies to prevent neuronal degeneration in diabetes and related neuropathies.
糖尿病是一种慢性病,有许多并发症,严重影响患者的生活质量。不同的神经病变可能会作为与神经系统相关的并发症出现,包括外周和中枢神经系统。这些神经元并发症的机制还远未阐明,但轴突运输损伤,这一对于神经元生理学至关重要的过程,在实验性糖尿病的背景下已经被描述。神经元细胞骨架和运动蛋白的改变、ATP 供应不足或神经炎症,这些干扰货物沿轴突有效运输的过程,被认为是导致轴突损伤的潜在原因,最终导致轴突退化。本综述的主要目的是汇集文献中主要的研究,探索可能与轴突运输缺陷相关的糖尿病诱导的改变,并呼吁人们关注进一步探索这一领域的极其重要性。了解糖尿病中神经元缺陷的机制对于开发新的治疗策略以预防糖尿病和相关神经病变中的神经元退化至关重要。