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論文
- タイトル
- タイトル（英）
- Pathogenetic mechanisms of amiodarone-induced peripheral neuropathy
- 参照URL
- https://researchmap.jp/213_nk/published_papers/46361731
- 著者
- 著者（英）
- Naoko Niimi,Hideji Yako,Shizuka Takaku,Kazunori Sango
- 担当区分
- 概要
- 概要（英）
- Amiodarone hydrochloride (AMD) has been prescribed for patients with refractory or life-threatening arrhythmias; however, its clinical use is often limited because of a number of side effects, such as corneal microdeposits, photosensitivity, pulmonary fibrosis, thyroid and liver dysfunction, and peripheral neuropathy. Although the incidence of peripheral neuropathy is less common than that of other abnormalities, long-term AMD therapy increases the risk of neurological manifestations. AMD-induced neuropathy is characterized by principally a sensorimotor demyelinating polyneuropathy, and nerve biopsies in patients with the neuropathy revealed loss of large myelinated fibers and prominent lysosomal inclusion bodies within Schwann cells. In our recent study, AMD dose-dependently induced cell death, lysosomal storage of phospholipids and neutral lipids, and oxidative stress in immortalized Schwann cells. The cytotoxicity and autophagy flux assays indicated that higher concentrations of AMD (10 M) inhibited the activities of lysosomal enzymes, thereby being a cause of the impaired degradation of autolysosomes in Schwann cells. Furthermore, AMD dose-dependently elicited detachment of Schwann cells from the neurite networks in neuron-Schwann cell coculture models. Taking these findings together with the previous in vivo studies, AMD-induced neuropathy may be, at least partly, attributed to the enhanced oxidative stress and deficient autolysosomal degradation in Schwann cells.
- 出版者・発行元
- 出版者・発行元（英）
- 誌名
- 誌名（英）
- Advances in Medicine and Biology. Volume 136
- 巻
- 136
- 号
- 開始ページ
- 41
- 終了ページ
- 62
- 出版年月
- 2019年1月2日
- 査読の有無
- 招待の有無
- 掲載種別
- 論文集(書籍)内論文
- ISSN
- DOI URL
- 共同研究・競争的資金等の研究課題