دورية أكاديمية

Exercise suppresses mouse systemic AApoAII amyloidosis through enhancement of the p38 MAPK signaling pathway

التفاصيل البيبلوغرافية
العنوان: Exercise suppresses mouse systemic AApoAII amyloidosis through enhancement of the p38 MAPK signaling pathway
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
الوصف
تدمد:17548403
17548411
DOI:10.1242/dmm.049327