Resistance Exercise Improves Mitochondrial Quality Control in a Rat Model of Sporadic Inclusion Body Myositis
| Autor: | Jung-Hoon Koo, Eun-Bum Kang, Joon-Yong Cho |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
Male
Aging medicine.medical_specialty Apoptosis Citrate (si)-Synthase Mitochondrion Myositis Inclusion Body chemistry.chemical_compound Physical Conditioning Animal Internal medicine Mitophagy medicine Animals Humans Citrate synthase Rats Wistar Muscle Skeletal Soleus muscle Amyloid beta-Peptides biology Superoxide Dismutase Chemistry Superoxide Chloroquine Resistance Training Catalase medicine.disease Muscle atrophy Mitochondria Muscle Rats Disease Models Animal Endocrinology Mitochondrial biogenesis Geriatrics biology.protein Geriatrics and Gerontology Inclusion body myositis medicine.symptom |
| Zdroj: | Gerontology. 65:240-252 |
| ISSN: | 1423-0003 0304-324X |
| DOI: | 10.1159/000494723 |
| Popis: | Background: Mitochondrial dysfunction is implicated in the pathogenesis of multiple muscular diseases, including sporadic inclusion body myositis (s-IBM), the most common aging-related muscle disease. However, the factors causing mitochondrial dysfunction in s-IBM are unknown. Objective: We hypothesized that resistance exercise (RE) may alleviate muscle impairment by improving mitochondrial function via reducing amyloid-beta (Aβ) accumulation. Methods: Twenty-four male Wistar rats were randomized to a saline-injection control group (sham, n = 8), a chloroquine (CQ) control group (CQ-CON, n = 8), and a CQ plus RE group (CQ-RE, n = 8) in which rats climbed a ladder with weight attached to their tails 9 weeks after starting CQ treatment. Results: RE markedly inhibited soleus muscle atrophy and muscle damage. RE reduced CQ-induced Aβ accumulation, which resulted in decreased formation of rimmed vacuoles and mitochondrial-mediated apoptosis. Most importantly, the decreased Aβ accumulation improved both mitochondrial quality control (MQC) through increased mitochondrial biogenesis and mitophagy, and mitochondrial dynamics. Furthermore, RE-mediated reduction of Aβ accumulation elevated mitochondrial oxidative capacity by upregulating superoxide dismutase-2, catalase, and citrate synthase via activating sirtuin 3 signaling. Conclusion: RE enhances mitochondrial function by improving MQC and mitochondrial oxidative capacity via reducing Aβ accumulation, thereby inhibiting CQ-induced muscle impairment, in a rat model of s-IBM. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|