Introduction Estrogens have crucial roles in an extensive range of physiological functions regulating cellular proliferation and differentiation, development, homeostasis, and metabolism ( Mauvais-Jarvis 2011 ). Estrogen insufficiency is
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Natalia Pavón, Alfredo Cabrera-Orefice, Juan Carlos Gallardo-Pérez, Cristina Uribe-Alvarez, Nadia A Rivero-Segura, Edgar Ricardo Vazquez-Martínez, Marco Cerbón, Eduardo Martínez-Abundis, Juan Carlos Torres-Narvaez, Raúl Martínez-Memije, Francisco-Javier Roldán-Gómez, and Salvador Uribe-Carvajal
Introduction Estrogens (17β-estradiol, estrone and progesterone) control diverse reproductive system functions. Their participation in other physiological processes such as cognition ( Sherwin 1999 ), cardiovascular function ( Stevenson 2000
H H Farman, K L Gustafsson, P Henning, L Grahnemo, V Lionikaite, S Movérare-Skrtic, J Wu, H Ryberg, A Koskela, J Tuukkanen, E R Levin, C Ohlsson, and M K Lagerquist
Introduction Estrogens are major regulators of skeletal growth and maintenance in both females and males ( Manolagas et al. 2013 , Vanderschueren et al. 2014 ). A decline in estrogen levels, as seen after menopause in women or after
Robert L Moore and Douglas V Faller
-mediated transcriptional repression and growth suppression of prostate cancer cells require SIRT1 ( Dai et al . 2007 ). It had not yet been determined whether SIRT1 plays a similar role in the action of estrogen antagonists. We here show that SIRT1 is not required for
Sara Merlo, Giuseppina Frasca, Pier Luigi Canonico, and Maria Angela Sortino
Introduction It is largely known that the regulatory roles of estrogen extend well beyond the reproductive system. In all tissues and cell types, estrogen exerts its actions by interacting with two specific receptor subtypes, α and β (ERs). These
M Merle Elloso, Kristen Phiel, Ruth A Henderson, Heather A Harris, and Steven J Adelman
2001 ). Although these gender differences are not fully understood, it is thought that sex hormonal influences on autoimmune disease may be involved. The disease modulating effects of estrogens in MS have been described. For example, clinical disease is
Alpha Dian-Yu Lin, Anita Mannikarottu, Barry A Kogan, Catherine Whitbeck, Paul Chichester, Robert E Leggett, and Robert M Levin
Introduction Postmenopausal urinary bladder dysfunctions including recurrent urinary tract infection and incontinence may be associated with decreased serum estrogen ( Hu et al. 2004 , Tinelli et al. 2005 ). One mechanism that
M J Meyer, A V Capuco, Y R Boisclair, and M E Van Amburgh
estrogenic compound ( Wallace 1953 ). These observations suggest that the effects of ovaries on the developing PAR are mediated by estrogen. The estrogen effects are mediated predominantly by the estrogen receptor α (ERα) in the mammary gland ( Couse
Shan-Jin Wang, Xin-Feng Li, Lei-Sheng Jiang, and Li-Yang Dai
several growth factors and hormones. One of the key regulators of endochondral bone development is estrogen ( Perry et al . 2008 ). Estrogen exerts its effect via traditional genomic interactions with two nuclear receptors, namely estrogen receptor α (ERα
K L Gustafsson, K H Nilsson, H H Farman, A Andersson, V Lionikaite, P Henning, J Wu, S H Windahl, U Islander, S Movérare-Skrtic, K Sjögren, H Carlsten, J-Å Gustafsson, C Ohlsson, and M K Lagerquist
Introduction Estrogen, the main female reproductive hormone, is a major regulator of bone homeostasis and it is well known that estrogen deficiency after menopause increases fracture risk and that estrogen treatment decreases this risk
