Mitochondria are no longer considered to be static structures that just make ATP. Emerging data show that mitochondrial form or shape is intimately related to mitochondrial function.1,2 It, therefore, follows that changes in mitochondrial substrate selection and metabolism might lead to altered mitochondrial dynamics. A recent study in Circulation Research examines this issue3 Article, see p 58 Diabetic cardiomyopathy is associated with cardiac lipotoxicity and mitochondrial dysfunction,4 and a better understanding of the mechanisms involved are needed. To examine the mechanisms linking lipid overload and diabetic cardiomyopathy, Tsushima et al3 studied a mouse model with overexpression of ACSL1 (long-chain acyl-CoA synthetase 1) in cardiomyocytes (ACS-transgenic [Tg]). ACSL1 was under the control of α-myosin heavy chain promoter, and the gene was, therefore, turned on shortly before birth. Wild-type (WT) hearts had little or no ACSL1 mRNA expression at postnatal day zero (P0), whereas ACS-Tg hearts expressed mRNA but no protein at this time (P0). An increase in ACSL1 protein was observed in the ACS-Tg hearts at ≈1 week, and by 12 weeks, there was >10-fold increase in ACSL1 in the transgenic hearts. Normally, after birth, there is an increase in mitochondrial dimensions, and the mitochondria become larger. Interestingly, the postnatal increase in mitochondrial dimensions is blunted in the ACS-Tg hearts. Two-dimensional electron microscopy showed that in WT hearts, mitochondrial dimensions doubled by 3 weeks after birth; however, this postnatal increase was not observed in ASC-Tg mice. To better assess mitochondrial differences, 3-dimensional transmission electron microscopy tomography was performed, and data collected at 8 weeks showed that ACS-Tg mitochondria were narrower and more elongated than mitochondria from WT hearts. Thus, a role for alterations in proteins that regulate mitochondrial dynamics, the mitochondrial fission and fusion proteins, were considered. As indicated by their names, these proteins regulate …

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线粒体不再被认为是仅构成ATP的静态结构。新兴数据表明，线粒体的形式或形状与线粒体功能密切相关。1,2因此，随之而来的是线粒体底物选择和代谢的变化可能导致线粒体动力学改变。Circulation Research的一项最新研究对此问题进行了研究3，请参见第58页糖尿病性心肌病与心脏脂质毒性和线粒体功能障碍有关4，还需要对其中涉及的机制有更好的了解。为了研究脂质超负荷与糖尿病性心肌病之间的联系机制，Tsshima等人[3]研究了一种在心肌细胞（ACS转基因[Tg]）中过表达ACSL1（长链酰基辅酶A合成酶1）的小鼠模型。ACSL1受α-肌球蛋白重链启动子的控制，因此，该基因在出生前不久就被打开了。野生型（WT）心脏在出生后第零天（P0）几乎没有ACSL1 mRNA表达，而ACS-Tg心脏此时没有mRNA（P0）表达。在约1周的ACS-Tg心脏中观察到ACSL1蛋白增加，到12周时，转基因心脏中的ACSL1增加> 10倍。通常，出生后线粒体尺寸增加，线粒体变大。有趣的是，ACS-Tg心脏中线粒体尺寸的出生后增加被抑制。二维电子显微镜显示，在野生型心脏中，线粒体尺寸在出生后3周增加了一倍。但是，在ASC-Tg小鼠中未观察到这种产后增加。为了更好地评估线粒体差异，进行了三维透射电子显微镜断层扫描，并在8周时收集的数据显示，ACS-Tg线粒体比来自WT心脏的线粒体更窄且更长。因此，考虑了改变调节线粒体动力学的蛋白质，线粒体裂变和融合蛋白中的作用。如其名称所示，这些蛋白质可调节……