| Item type |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2021-11-12 |
| タイトル |
|
|
タイトル |
Reduction of Superoxide Dismutase 1 Delays Regeneration of Cardiotoxin-Injured Skeletal Muscle in KK/Ta-Ins2Akita Mice with Progressive Diabetic Nephropathy |
|
言語 |
en |
| 言語 |
|
|
言語 |
eng |
| 主題 |
|
|
主題Scheme |
Other |
|
主題 |
akita mouse |
| 主題 |
|
|
主題Scheme |
Other |
|
主題 |
cardiotoxin injury |
| 主題 |
|
|
主題Scheme |
Other |
|
主題 |
diabetic nephropathy |
| 主題 |
|
|
主題Scheme |
Other |
|
主題 |
muscle regeneration |
| 主題 |
|
|
主題Scheme |
Other |
|
主題 |
oxidative stress |
| 主題 |
|
|
主題Scheme |
Other |
|
主題 |
superoxide dismutase 1 |
| 資源タイプ |
|
|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
|
資源タイプ |
journal article |
| アクセス権 |
|
|
アクセス権 |
open access |
|
アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
| 作成者 |
Takahashi, Yuya
Shimizu, Tatsunori
Kato, Shunsuke
Nara, Mitsuhiko
Suganuma, Yumi
Sato, Takehiro
Morii, Tsukasa
Yamada, Yuichiro
Fujita, Hiroki
|
| 内容記述 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
Superoxide dismutase (SOD) is a major antioxidant enzyme for superoxide removal, and cytoplasmic SOD (SOD1) is expressed as a predominant isoform in all cells. We previously reported that renal SOD1 deficiency accelerates the progression of diabetic nephropathy (DN) via increasing renal oxidative stress. To evaluate whether the degree of SOD1 expression determines regeneration capacity and sarcopenic phenotypes of skeletal muscles under incipient and advanced DN conditions, we investigated the alterations of SOD1 expression, oxidative stress marker, inflammation, fibrosis, and regeneration capacity in cardiotoxin (CTX)-injured tibialis anterior (TA) muscles of two Akita diabetic mouse models with different susceptibility to DN, DN-resistant C57BL/6-Ins2Akita and DNprone KK/Ta-Ins2Akita mice. Here, we report that KK/Ta-Ins2Akita mice, but not C57BL/6-Ins2Akita mice, exhibit delayed muscle regeneration after CTX injection, as demonstrated by the finding indicating significantly smaller average cross-sectional areas of regenerating TA muscle myofibers relative to KK/Ta-wild-type mice. Furthermore, we observed markedly reduced SOD1 expression in CTX-injected TA muscles of KK/Ta-Ins2Akita mice, but not C57BL/6-Ins2Akita mice, along with increased inflammatory cell infiltration, prominent fibrosis and superoxide overproduction. Our study provides the first evidence that SOD1 reduction and the following superoxide overproduction delay skeletal muscle regeneration through induction of overt inflammation and fibrosis in a mouse model of progressive DN. |
|
言語 |
en |
| 出版タイプ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| 書誌情報 |
International Journal of Molecular Sciences
巻 22,
号 11,
p. 5491,
発行日 2021
|
| 収録物識別子 |
|
|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
1422-0067 |
| 出版者 |
|
|
出版者 |
MDPI |
| 関連情報 |
|
|
関連タイプ |
isIdenticalTo |
|
|
識別子タイプ |
DOI |
|
|
関連識別子 |
https://doi.org/10.3390/ijms22115491 |
| 権利情報 |
|
|
権利情報 |
© 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/). |
iA_2021_37 (2.3 MB)
