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首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >Aerobic Exercise Training Induces the Mitonuclear Imbalance and UPRmt in the Skeletal Muscle of Aged Mice
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Aerobic Exercise Training Induces the Mitonuclear Imbalance and UPRmt in the Skeletal Muscle of Aged Mice

机译：有氧运动训练在老年小鼠的骨骼肌中诱导Qualual核心不平衡和UPRMT

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The impairment of the mitochondrial functions is a hallmark of aging. During aging, there is a downregulation of two mechanisms strictly associated with mitochondrial integrity, including the mitonuclear imbalance (eg, imbalance in mitochondrial- versus nuclear-encoded mitochondrial proteins) and the mitochondrial unfolded protein response (UPRmt). Here, we evaluated the effects of aerobic exercise in the mitonuclear imbalance and UPRmt markers in the skeletal muscle of old mice. We combined the physiological tests, molecular and bioinformatic analyzes to evaluate the effects of 4 weeks of aerobic exercise training on mitonuclear imbalance and UPRmt markers in the skeletal muscle of young (2 months) and aged (24 months) C57BL/6J mice. Initially, we found that aging reduced several mitochondrial genes in the gastrocnemius muscle, and it was accompanied by the low levels of UPRmt markers, including Yme1l1 and Clpp mRNA. As expected, physical training improved the whole-body metabolism and physical performance of aged mice. The aerobic exercise increased key proteins involved in the mitochondrial biogenesis/functions (VDAC and SIRT1) along with mitochondrial-encoded genes (mtNd1, mtCytB, and mtD-Loop) in the skeletal muscle of old mice. Interestingly, aerobic exercise induced the mitonuclear imbalance, increasing MTCO1/ATP5a ratio and UPRmt markers in the skeletal muscle, including HSP60, Lonp1, and Yme1L1 protein levels in the gastrocnemius muscle of aged mice. These data demonstrate that aerobic exercise training induced mitonuclear imbalance and UPRmt in the skeletal muscle during aging. These phenomena could be involved in the improvement of the mitochondrial metabolism and oxidative capacity in aged individuals.
机译：线粒体功能受损是衰老的标志。在衰老过程中，有两种机制与线粒体完整性密切相关，包括有丝分裂核失衡（例如，线粒体与核编码线粒体蛋白的失衡）和线粒体未折叠蛋白反应（UPRmt）。在这里，我们评估了有氧运动对老年小鼠骨骼肌有丝分裂核失衡和UPRmt标记物的影响。我们结合生理测试、分子和生物信息学分析，评估4周有氧运动训练对年轻（2个月）和老年（24个月）C57BL/6J小鼠骨骼肌有丝分裂核失衡和UPRmt标记物的影响。最初，我们发现衰老减少了腓肠肌中的几个线粒体基因，并且伴随着UPRmt标记物的低水平，包括Yme1l1和Clpp mRNA。正如预期的那样，体育锻炼改善了老龄小鼠的全身代谢和身体机能。有氧运动增加了参与老年小鼠骨骼肌线粒体生物发生/功能（VDAC和SIRT1）以及线粒体编码基因（mtNd1、mtCytB和mtD环）的关键蛋白质。有趣的是，有氧运动导致有丝分裂核失衡，增加骨骼肌中的MTCO1/ATP5a比率和UPRmt标记物，包括老年小鼠腓肠肌中的HSP60、Lonp1和Yme1L1蛋白水平。这些数据表明，有氧运动训练导致衰老期间骨骼肌有丝分裂核失衡和UPRmt。这些现象可能与老年人线粒体代谢和氧化能力的改善有关。

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