دورية أكاديمية
Inflammatory Cytokine-Induced Muscle Atrophy and Weakness Can Be Ameliorated by an Inhibition of TGF-β-Activated Kinase-1
| العنوان: | Inflammatory Cytokine-Induced Muscle Atrophy and Weakness Can Be Ameliorated by an Inhibition of TGF-β-Activated Kinase-1 |
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| المؤلفون: | Mai Kanai, Byambasuren Ganbaatar, Itsuro Endo, Yukiyo Ohnishi, Jumpei Teramachi, Hirofumi Tenshin, Yoshiki Higa, Masahiro Hiasa, Yukari Mitsui, Tomoyo Hara, Shiho Masuda, Hiroki Yamagami, Yuki Yamaguchi, Ken-ichi Aihara, Mayu Sebe, Rie Tsutsumi, Hiroshi Sakaue, Toshio Matsumoto, Masahiro Abe |
| المصدر: | International Journal of Molecular Sciences, Vol 25, Iss 11, p 5715 (2024) |
| بيانات النشر: | MDPI AG, 2024. |
| سنة النشر: | 2024 |
| المجموعة: | LCC:Biology (General) LCC:Chemistry |
| مصطلحات موضوعية: | TAK1 inhibitor, myostatin, MyoD1, TNF-α, IL-1β, Biology (General), QH301-705.5, Chemistry, QD1-999 |
| الوصف: | Chronic inflammation causes muscle wasting. Because most inflammatory cytokine signals are mediated via TGF-β-activated kinase-1 (TAK1) activation, inflammatory cytokine-induced muscle wasting may be ameliorated by the inhibition of TAK1 activity. The present study was undertaken to clarify whether TAK1 inhibition can ameliorate inflammation-induced muscle wasting. SKG/Jcl mice as an autoimmune arthritis animal model were treated with a small amount of mannan as an adjuvant to enhance the production of TNF-α and IL-1β. The increase in these inflammatory cytokines caused a reduction in muscle mass and strength along with an induction of arthritis in SKG/Jcl mice. Those changes in muscle fibers were mediated via the phosphorylation of TAK1, which activated the downstream signaling cascade via NF-κB, p38 MAPK, and ERK pathways, resulting in an increase in myostatin expression. Myostatin then reduced the expression of muscle proteins not only via a reduction in MyoD1 expression but also via an enhancement of Atrogin-1 and Murf1 expression. TAK1 inhibitor, LL-Z1640-2, prevented all the cytokine-induced changes in muscle wasting. Thus, TAK1 inhibition can be a new therapeutic target of not only joint destruction but also muscle wasting induced by inflammatory cytokines. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 25115715 1422-0067 1661-6596 |
| Relation: | https://www.mdpi.com/1422-0067/25/11/5715; https://doaj.org/toc/1661-6596; https://doaj.org/toc/1422-0067 |
| DOI: | 10.3390/ijms25115715 |
| URL الوصول: | https://doaj.org/article/9598cba046254671827402faa5ef1389 |
| رقم الأكسشن: | edsdoj.9598cba046254671827402faa5ef1389 |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 25115715 14220067 16616596 |
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| DOI: | 10.3390/ijms25115715 |