Aerobic interval training attenuates mitochondrial dysfunction in rats post-myocardial infarction: roles of mitochondrial network dynamics.
Aerobic interval training attenuates mitochondrial dysfunction in rats post-myocardial infarction: roles of mitochondrial network dynamics.
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DOI：
10.3390/ijms15045304
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发表时间：
2014-03-26
影响因子：
5.6
通讯作者：
Zang WJ
中科院分区：
文献类型：
--
作者：
Jiang HK;Wang YH;Sun L;He X;Zhao M;Feng ZH;Yu XJ;Zang WJ
有氧间歇训练（AIT）对心血管疾病有良好的影响。然而，AIT对心肌梗死（MI）后相关线粒体功能障碍的影响仍不清楚。在这项研究中，我们研究了AIT对心肌梗死后大鼠心肌线粒体的保护作用，重点是线粒体动力学（融合和分裂）。线粒体呼吸功能（通过呼吸控制率（RCR）和ADP与耗氧量（P/O）的比值测量）;复合物活性;动态蛋白质核过氧化物酶体增殖物激活受体γ辅激活因子1-α（PGC-1α）;观察细胞外信号调节激酶（ERK）1/2、c-Jun氨基末端蛋白激酶（JNK）和P53的氧化信号通路。MI后大鼠表现出线粒体功能障碍和不利的线粒体网络动力学（融合减少和分裂增加），这与ERK 1/2-JNK-P53信号转导激活和核PGC-1α减少有关。AIT后，MI相关的线粒体功能障碍得到改善（RCR和P/O升高，复合物I、III和IV活性增强）;此外，还观察到融合（mfn 2和OPA 1）增加、裂变（DRP 1）减少、核PGC-1α升高和ERK 1/2-JNK-P53信号转导失活。这些结果表明，AIT可通过抑制心肌梗死后线粒体的动力学病理性重构来恢复线粒体功能，其机制可能与ERK 1/2-JNK-P53信号通路失活和核PGC-1α表达增加有关。
Aerobic interval training (AIT) can favorably affect cardiovascular diseases. However, the effects of AIT on post-myocardial infarction (MI)—associated mitochondrial dysfunctions remain unclear. In this study, we investigated the protective effects of AIT on myocardial mitochondria in post-MI rats by focusing on mitochondrial dynamics (fusion and fission). Mitochondrial respiratory functions (as measured by the respiratory control ratio (RCR) and the ratio of ADP to oxygen consumption (P/O)); complex activities; dynamic proteins (mitofusin (mfn) 1/2, type 1 optic atrophy (OPA1) and dynamin-related protein1 (DRP1)); nuclear peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α); and the oxidative signaling of extracellular signal-regulated kinase (ERK) 1/2, c-Jun NH2-terminal protein kinase (JNK) and P53 were observed. Post-MI rats exhibited mitochondrial dysfunction and adverse mitochondrial network dynamics (reduced fusion and increased fission), which was associated with activated ERK1/2-JNK-P53 signaling and decreased nuclear PGC-1α. After AIT, MI-associated mitochondrial dysfunction was improved (elevated RCR and P/O and enhanced complex I, III and IV activities); in addition, increased fusion (mfn2 and OPA1), decreased fission (DRP1), elevated nuclear PGC-1α and inactivation of the ERK1/2-JNK-P53 signaling were observed. These data demonstrate that AIT may restore the post-MI mitochondrial function by inhibiting dynamics pathological remodeling, which may be associated with inactivation of ERK1/2-JNK-P53 signaling and increase in nuclear PGC-1α expression.
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影响因子：
10.8
作者：
Chen, Le;Gong, Qizhi;Knowlton, Anne A.
通讯作者：
Knowlton, Anne A.
影响因子：
37.8
作者：
Cheng XW;Kuzuya M;Kim W;Song H;Hu L;Inoue A;Nakamura K;Di Q;Sasaki T;Tsuzuki M;Shi GP;Okumura K;Murohara T
通讯作者：
Murohara T
运动训练恢复心力衰竭中心力衰竭的心脏蛋白质质量控制。
影响因子：
3.7
作者：
Campos JC;Queliconi BB;Dourado PM;Cunha TF;Zambelli VO;Bechara LR;Kowaltowski AJ;Brum PC;Mochly-Rosen D;Ferreira JC
通讯作者：
Ferreira JC
DOI：
10.1016/j.bbrc.2008.09.018
发表时间：
2008-11-21
影响因子：
3.1
作者：
Cheng, Yan;Qiu, Feng;Ikejima, Takashi
通讯作者：
Ikejima, Takashi
影响因子：
6.6
作者：
Feng, Zhihui;Zou, Xuan;Liu, Jiankang
通讯作者：
Liu, Jiankang