Department of Immunology, Nagoya University Graduate School of Medicine, 65 Turumai-cho, Showa-ku, Nagoya, Aichi, 466-8520, Japan.
Exp Gerontol. 2013 Mar;48(3):341-8. doi: 10.1016/j.exger.2013.01.005. Epub 2013 Jan 18.
The specific processes that cause aging of the cardiac tissue remain elusive. C57BL/6 (B6) mice are commonly used for investigating age-related diseases in mammals. We thus sought to evaluate the cardiac aging process in B6 mice. Cardiac tissues from the newborn (B6 NB), 2month-old (B6 2M) and 21-27month-old B6 mice (B6 aged) were used for the investigation. Several age-related cellular processes were evaluated, including telomere shortening, changes in p53 and p16 expression, changes in mitochondria DNA expression and DNA deletion, and alteration of mitochondria. We found that the aging of the B6 mice cardiac tissue is associated with the maintenance of telomere length, increased expression of p53 and p16, mild changes in mitochondrial DNA expression but widespread DNA deletion, and significant alterations of the mitochondrial ultrastructure within the cardiac tissue. The results of our studies suggest that mitochondrial DNA deletions, which affect the mitochondrial ultrastructure, cytochrome C oxidase activity, and p53 expression, are significantly associated with cardiac aging and may be a source of age-related heart failure.
导致心脏组织衰老的具体过程仍然难以捉摸。C57BL/6（B6）小鼠常用于研究哺乳动物的与年龄相关的疾病。因此，我们试图评估 B6 小鼠的心脏衰老过程。使用来自新生（B6 NB）、2 月龄（B6 2M）和 21-27 月龄 B6 小鼠（B6 老年）的心脏组织进行研究。评估了几种与年龄相关的细胞过程，包括端粒缩短、p53 和 p16 表达的变化、线粒体 DNA 表达和 DNA 缺失的变化以及线粒体的改变。我们发现，B6 小鼠心脏组织的衰老与端粒长度的维持、p53 和 p16 表达的增加、线粒体 DNA 表达的轻微变化但广泛的 DNA 缺失以及心脏组织中线粒体超微结构的显著改变有关。我们的研究结果表明，影响线粒体超微结构、细胞色素 C 氧化酶活性和 p53 表达的线粒体 DNA 缺失与心脏衰老显著相关，可能是与年龄相关的心力衰竭的一个来源。
