TY - JOUR
T1 - Regulation of mitochondrial respiratory chain structure and function by estrogens/estrogen receptors and potential physiological/pathophysiological implications
AU - Chen, Jin Qiang
AU - Yager, James D.
AU - Russo, Jose
N1 - Funding Information:
Parts of the research work conducted by the authors (JQC and JDY) in Johns Hopkins Bloomberg School of Public Health that were described in the manuscript were supported by U.S. PHS grants CA36701 and CA77550 (to JDY). Authors are grateful to Dr. Terry Brown of Johns Hopkins Bloomberg School of Public Health and to Dr. Edward T. Morgan of Emory University School of Medicine for their previous review of parts of the manuscript.
PY - 2005/10/30
Y1 - 2005/10/30
N2 - It is well known that the biological and carcinogenic effects of 17β-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, E 2-mediated cardiovascular and neuroprotective effects in target cells are also discussed.
AB - It is well known that the biological and carcinogenic effects of 17β-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, E 2-mediated cardiovascular and neuroprotective effects in target cells are also discussed.
KW - 17β-estradiol
KW - Estrogen
KW - Estrogen carcinogenesis
KW - Estrogen receptors α and β
KW - Mitochondria
KW - Mitochondrial DNA transcription
KW - Mitochondrial DNA-encoded gene
KW - Mitochondrial estrogen receptor
KW - Mitochondrial respiratory chain (MRC)
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U2 - 10.1016/j.bbamcr.2005.08.001
DO - 10.1016/j.bbamcr.2005.08.001
M3 - Review article
C2 - 16169101
AN - SCOPUS:26944439050
SN - 0167-4889
VL - 1746
SP - 1
EP - 17
JO - Biochimica et Biophysica Acta - Molecular Cell Research
JF - Biochimica et Biophysica Acta - Molecular Cell Research
IS - 1
ER -