دورية أكاديمية
Exercise suppresses mouse systemic AApoAII amyloidosis through enhancement of the p38 MAPK signaling pathway
العنوان: | Exercise suppresses mouse systemic AApoAII amyloidosis through enhancement of the p38 MAPK signaling pathway |
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المؤلفون: | Xiaoran Cui, Jinko Sawashita, Jian Dai, Chang Liu, Yuichi Igarashi, Masayuki Mori, Hiroki Miyahara, Keiichi Higuchi |
المصدر: | Disease Models & Mechanisms, Vol 15, Iss 3 (2022) |
بيانات النشر: | The Company of Biologists, 2022. |
سنة النشر: | 2022 |
المجموعة: | LCC:Medicine LCC:Pathology |
مصطلحات موضوعية: | amyloidosis, exercise, mouse model, heat shock protein beta-1, p38 mapk signaling pathway, rna-seq analysis, Medicine, Pathology, RB1-214 |
الوصف: | Exercise interventions are beneficial for reducing the risk of age-related diseases, including amyloidosis, but the underlying molecular links remain unclear. Here, we investigated the protective role of interval exercise training in a mouse model of age-related systemic apolipoprotein A-II amyloidosis (AApoAII) and identified potential mechanisms. Mice subjected to 16 weeks of exercise showed improved whole-body physiologic functions and exhibited substantial inhibition of amyloidosis, particularly in the liver and spleen. Exercise activated the hepatic p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway and the downstream transcription factor tumor suppressor p53. This activation resulted in elevated expression and phosphorylation of heat shock protein beta-1 (HSPB1), a chaperone that defends against protein aggregation. In amyloidosis-induced mice, the hepatic p38 MAPK-related adaptive responses were additively enhanced by exercise. We observed that with exercise, greater amounts of phosphorylated HSPB1 accumulated at amyloid deposition areas, which we suspect inhibits amyloid fibril formation. Collectively, our findings demonstrate the exercise-activated specific chaperone prevention of amyloidosis, and suggest that exercise may amplify intracellular stress-related protective adaptation pathways against age-associated disorders, such as amyloidosis. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 1754-8403 1754-8411 |
Relation: | http://dmm.biologists.org/content/15/3/dmm049327; https://doaj.org/toc/1754-8403; https://doaj.org/toc/1754-8411 |
DOI: | 10.1242/dmm.049327 |
URL الوصول: | https://doaj.org/article/f6ed756bb15543a299b4f7d1faedba41 |
رقم الأكسشن: | edsdoj.f6ed756bb15543a299b4f7d1faedba41 |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 17548403 17548411 |
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DOI: | 10.1242/dmm.049327 |