Short-Duration Swimming Exercise after Myocardial Infarction Attenuates Cardiac Dysfunction and Regulates Mitochondrial Quality Control in Aged Mice.
Short-Duration Swimming Exercise after Myocardial Infarction Attenuates Cardiac Dysfunction and Regulates Mitochondrial Quality Control in Aged Mice.
复制标题
心肌梗塞后的短期游泳运动可减轻老年小鼠的心脏功能障碍并调节线粒体质量控制
DOI：
10.1155/2018/4079041
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发表时间：
2018
影响因子：
--
通讯作者：
Gao F
中科院分区：
文献类型：
--
作者：
Zhao D;Sun Y;Tan Y;Zhang Z;Hou Z;Gao C;Feng P;Zhang X;Yi W;Gao F
背景运动对稳定性心肌梗死（MI）后心脏康复（CR）的益处。老年冠心病患者适宜的运动时间仍存在争议，其分子机制尚不清楚。方法和结果18月龄稳定型心肌梗死小鼠随机接受不同持续时间的运动训练，包括15和60 min游泳训练（ST），每天1次，每周5次，共8周。与安静的小鼠相比，15分钟ST，而不是60分钟ST，显著增强左心室功能，增加存活率，抑制心肌纤维化和凋亡。ST 15 min通过调节线粒体分裂-融合信号改善线粒体形态。ST 15 min通过抑制LC 3-II和P62水平以及增加PINK/Parkin表达来调节线粒体自噬信号传导。15 min ST也抑制ROS的产生并增强抗氧化剂SOD 2的活性。值得注意的是，15分钟ST显著增加体内sirtuin（SIRT）3水平（2.7倍），而SIRT 3的抑制加剧了缺氧下衰老H9 c2细胞LDH释放和ROS产生。此外，SIRT 3沉默损害衰老心肌细胞对抗模拟缺血（SI）损伤的线粒体动力学和线粒体自噬。总的来说，我们的研究首次证明，持续的短期运动，而不是长期运动，减轻老年小鼠心肌梗死后心功能不全。很可能是由短时间ST方案诱导的对升高的SIRT 3蛋白水平的正调节改善了线粒体质量控制，并减少了细胞凋亡和纤维化，从而导致了观察到的更耐药的表型。
Background Exercise benefits to cardiac rehabilitation (CR) following stable myocardial infarction (MI). The suitable exercise duration for aged patients with coronary heart disease (CHD) remains controversial, and the underlying molecular mechanism is still unclear. Methods and Results 18-Month-old mice after stable MI were randomly submitted to different durations of exercise, including 15 and 60 min swimming training (ST) once per day, five times a week for 8 weeks. Compared to sedentary mice, 15 min ST, rather than 60 min ST, significantly augmented left ventricular function, increased survival rate, and suppressed myocardial fibrosis and apoptosis. 15 min ST improved mitochondrial morphology via regulating mitochondrial fission-fusion signaling. 15 min ST regulated mitophagy signaling via inhibiting LC3-II and P62 levels and increasing PINK/Parkin expression. 15 min ST also inhibited ROS production and enhanced antioxidant SOD2 activity. Notably, 15 min ST significantly increased sirtuin (SIRT) 3 level (2.7-fold) in vivo while the inhibition of SIRT3 exacerbated senescent H9c2 cellular LDH release and ROS production under hypoxia. In addition, SIRT3 silencing impairs mitochondrial dynamics and mitophagy in senescent cardiomyocytes against simulated ischemia (SI) injury. Conclusion Collectively, our study demonstrated for the first time that sustained short-duration exercise, rather than long-duration exercise, attenuates cardiac dysfunction after MI in aged mice. It is likely that the positive regulation induced by a short-duration ST regimen on the elevated SIRT3 protein level improved mitochondrial quality control and decreased apoptosis and fibrosis contributed to the observed more resistant phenotype.
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影响因子：
64.5
作者：
López-Otín C;Blasco MA;Partridge L;Serrano M;Kroemer G
通讯作者：
Kroemer G
DOI：
10.1126/science.1201940
发表时间：
2011-08-26
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Green DR;Galluzzi L;Kroemer G
通讯作者：
Kroemer G
DOI：
10.1073/pnas.92.20.9363
发表时间：
1995-09-26
影响因子：
11.1
作者：
DIMRI, GP;LEE, XH;CAMPISI, J
通讯作者：
CAMPISI, J
DOI：
10.1152/ajpheart.00075.2014
发表时间：
2014-04-01
影响因子：
4.8
作者：
Collins, Helen E.;He, Lan;Chatham, John C.
通讯作者：
Chatham, John C.
DOI：
10.1083/jcb.200910140
发表时间：
2010-04-19
期刊：
The Journal of cell biology
影响因子：
--
作者：
Matsuda N;Sato S;Shiba K;Okatsu K;Saisho K;Gautier CA;Sou YS;Saiki S;Kawajiri S;Sato F;Kimura M;Komatsu M;Hattori N;Tanaka K
通讯作者：
Tanaka K