Leydig cell steroidogenesis unexpectedly escapes mitochondrial dysfunction in prematurely aging mice.
第一作者:
Irina G,Shabalina
第一单位:
*Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden; Department of Women's and Children's Health, Pediatric Endocrinology Unit, Astrid Lindgren's Children Hospital, Stockholm, Sweden; Department of Laboratory Medicine, Karolinska Institutet, Huddinge, Sweden; and Institute of Experimental Morphology, Pathology and Anthropology with Museum, Sofia, Bulgaria.
作者:
医学主题词
衰老(Aging);动物(Animals);细胞色素b5类(Cytochromes b5);细胞色素c类(Cytochromes c);DNA, 线粒体(DNA, Mitochondrial);莱迪希细胞(Leydig Cells);男(雄)性(Male);膜电位, 线粒体(Membrane Potential, Mitochondrial);小鼠(Mice);小鼠, 近交C57BL(Mice, Inbred C57BL);线粒体(Mitochondria);线粒体疾病(Mitochondrial Diseases);活性氧(Reactive Oxygen Species);精子(Spermatozoa);睾酮(Testosterone)
DOI
10.1096/fj.15-271825
PMID
25900807
发布时间
2015-08-03
- 浏览12
FASEB journal
3274-86页
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