Regulation of mitochondrial respiratory chain structure and function by estrogens/estrogen receptors and potential physiological/pathophysiological implications

被引:150
作者
Chen, JQ
Yager, JD
Russo, J
机构
[1] Fox Chase Canc Ctr, Breast Canc Res Lab, Philadelphia, PA 19111 USA
[2] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Environm Hlth Sci, Div Toxicol Sci, Baltimore, MD 21205 USA
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH | 2005年 / 1746卷 / 01期
关键词
17; beta-estradiol; estrogen; estrogen carcinogenesis; estrogen receptors alpha and beta; mitochondria; mitochondrial DNA-encoded gene; mitochondrial DNA transcription; mitochondrial estrogen receptor; mitochondrial respiratory chain (MRC); nuclear genes for MRC protein;
D O I
10.1016/j.bbamcr.2005.08.001
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
It is well known that the biological and carcinogenic effects of 17 beta-estradiol (E-2) are mediated via nuclear estrogen receptors (ERs) by regulating nuclear gene expression. Several rapid, non-nuclear genomic effects of E-2 are mediated via plasma membrane-bound ERs. In addition, there is accumulating evidence suggesting that mitochondria are also important targets for the action of estrogens and ERs. This review summarized the studies on the effects of estrogens via ERs on mitochondrial structure and function. The potential physiological and pathophysiological implications of deficiency and/or overabundance of these E-2/ER-mediated mitochondrial effects in stimulation of cell proliferation, inhibition of apoptosis, E-2-mediated cardiovascular and neuroprotective effects in target cells are also discussed. (c) 2005 Elsevier B.V All rights reserved.
引用
收藏
页码:1 / 17
页数:17
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