Regulation of mitochondrial respiratory chain structure and function by estrogens/estrogen receptors and potential physiological/pathophysiological implications.
It is well known that the biological and carcinogenic effects of 17beta-estradiol (E2) are mediated via nuclear estrogen receptors (ERs) by regulating nuclear gene expression. Several rapid, non-nuclear genomic effects of E2 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 E2/ER-mediated mitochondrial effects in stimulation of cell proliferation, inhibition of apoptosis, E2-mediated cardiovascular and neuroprotective effects in target cells are also discussed.
Chen
Jin-Qiang
JQ
Breast Cancer Research Laboratory, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111, USA. jinqiang.chen@fccc.edu
Yager
James D
JD
Russo
Jose
J
D000818:Animals; D004272:DNA, Mitochondrial / Q000235:genetics; D004579:Electron Transport / Q000502:physiology*; D004967:Estrogens / Q000378:metabolism*; D005786:Gene Expression Regulation; D006801:Humans; D008928:Mitochondria / Q000737:chemistry* / Q000235:genetics / Q000378:metabolism*; D011960:Receptors, Estrogen / Q000378:metabolism*
D004272:DNA, Mitochondrial; D004967:Estrogens; D011960:Receptors, Estrogen