کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5514225 1541593 2017 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Effect of nitric oxide to axonal degeneration in multiple sclerosis via downregulating monocarboxylate transporter 1 in oligodendrocytes
ترجمه فارسی عنوان
اثر اکسید نیتریک به دژنراسیون آکسون در مولتیپل اسکلروزیس از طریق کاهش دهنده ترانسفورمر 1 مونوکربوک سیلات در الیگودندروستیک
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
چکیده انگلیسی


- Analyzed the mechanism how NO induces mitochondrial dysfunction in neurons and glial cells from a balanced view.
- Described the role of MCT1 in energy mechanism of MS, and decrease of MCT1 may account for axonal energy deficit.
- Hypothesized that NO-induced MCT1 downregulation in OLs may involve in axonal degeneration, and eventually leads to MS.

Multiple sclerosis (MS) is a neurodegenerative disease of the central nervous system (CNS). Axonal degeneration, one of the main pathological characteristics of MS, is affected by nitric oxide (NO). In turn, NO induces mitochondrial dysfunction of neurons and glial cells. Inadequate glucose causes monocarboxylate transporter 1 (MCT1) to transfer lactate from oligodendrocytes (OLs) to neurons, which decreases MCT1 and results in energy substrate deficit (mainly lactate) in axons. The condition gradually leads to axonal degeneration. This study proposes that NO-induced MCT1 down-regulation in OLs may be involved in the pathological process of axonal degeneration, which eventually leads to MS.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Nitric Oxide - Volume 67, 1 July 2017, Pages 75-80
نویسندگان
, , , ,