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Hormones and Cardiovascular Disease
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
Estrogen exerts its effects through classical endocrinology, intracrinology, and a network of estrogen receptors (estrogen receptor alpha, estrogen receptor beta, and GPER). Metabolic effects of estrogen are primarily driven through estrogen receptor alpha (ERα), though the precise mechanisms are still under investigation.69 Imbalance in the metabolic network of estrogen receptors ERα/ERβ may promote metabolic syndrome via insulin signaling.70
Chemopreventive Agents
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
Increased levels of circulating estrogen have been shown to enhance the risk of developing breast and endometrial cancers, with approximately 70% of breast cancers categorized as estrogen-receptor (ER) positive and that can be treated with antiestrogen therapies. Estrogen has been shown to play a vital role in the early-stage development and proliferation of epithelial cells that precedes ER-positive invasive breast cancer. Estrogen can increase the risk of breast and endometrial cancers via several different molecular mechanisms, including a reduced level of apoptosis. The situation is further complicated by the fact that, although Estrogen Receptor Alpha (ER-α) is elevated in several cancer cell types and acts to induce cellular proliferation, Estrogen Receptor Beta (ER-β) has demonstrated protective effects by inhibiting proliferation.
Current and emerging pharmacological agents in the treatment of osteoporosis
Published in Peter V. Giannoudis, Thomas A. Einhorn, Surgical and Medical Treatment of Osteoporosis, 2020
James X. Liu, Thomas A. Einhorn
Raloxifene exerts its action as either an estrogen agonist or antagonist depending on the specific tissue that it targets. There are two primary isoforms of estrogen receptors: estrogen receptor alpha (ERα), which is primarily an activating receptor, and estrogen receptor beta (ERβ), which is primarily an inhibiting receptor (6). ERβ exerts its inhibitory action on ERα by forming a heterodimer. Thus, the levels of expression that are unique to a particular tissue type have different levels of isoforms that will direct cellular responsiveness to estrogens. In general, raloxifene functions as an estrogen agonist in bone and lipid metabolism and functions as an estrogen antagonist in breast and uterine tissue.
The role of anti-proliferative effects of atorvastatin on uterine fibroids: findings from a clinical study
Published in Gynecological Endocrinology, 2021
Masoumeh Ghafarzadeh, Amir Shakarami, Fatemeh Yari, Zahra Marzban Rad
Laufs et al. [26] reported that low doses of statin stimulate angiogenesis through increased nitric oxide (NO) production, whereas these compounds at high doses reduce protein prenylation and inhibit cell growth. Thus, there seems to be a different (non-estrogen-dependent) pathway in leiomyoma stimulation. Genetic factors, steroid hormones and growth factors are involved in fibroid formation and growth. It is also reported that estrogen in the presence of the estrogen receptor alpha, stimulates cell proliferation and has anti-apoptotic effects. According to the results of studies, estrogen has been shown to increase fibroid growth. Progesterone has also been shown to increase the growth of uterine fibroids. Similarly, expression of progesterone receptor is upregulated in these tissues as compared to normal uterine tissues. As stated, statins inhibit cholesterol synthesis that is also a precursor for the production of steroid hormones such as estrogen and progesterone. Hence, statins are able to reduce the synthesis androgens [27], which can be one of the possible mechanisms of statins for the reduction of fibroid size.
Prediagnostic use of estrogen-only therapy is associated with improved colorectal cancer survival in menopausal women: a Swedish population-based cohort study
Published in Acta Oncologica, 2021
Johanna Simin, Qing Liu, Xinchen Wang, Katja Fall, Cecilia Williams, Steven Callens, Lars Engstrand, Nele Brusselaers
In addition to lower incidence among women, CRC-mortality is one-fourth lower among women than men, indicating for a potential role of sex hormones (and particularly estrogens) in CRC progression [1,3,4]. Two nuclear receptors, estrogen receptor alpha (ERα) and beta (ERβ) mediate effects of estrogen. ERβ in normal colon epithelia has been experimentally shown to play a role in the prevention of a tumor formation in mouse models, by reducing inflammation of the gut [5]. Furthermore, in-vivo mice-models suggest exogenous estrogens impacting inflammatory markers and reducing proliferation of the crypt [5,6], and changing gut microbiota diversity in CRC-induced males [7]. As this posed link of estrogens with gut inflammation and microbiome might be modifiable, it could contribute to a reduced CRC risk [7], and potentially improved survival.
Denosumab for cancer-related bone loss
Published in Expert Opinion on Biological Therapy, 2020
Emanuela Dell’Aquila, Grazia Armento, Michele Iuliani, Sonia Simonetti, Loretta D’Onofrio, Tea Zeppola, Cristina Madaudo, Marco Russano, Fabrizio Citarella, Giulia Ribelli, Francesco Pantano, Bruno Vincenzi, Giuseppe Tonini, Daniele Santini
Similar to androgens, estrogens promote bone formation through Estrogen Receptor alpha and beta (ERα and ERβ), both expressed by OBs and OCs. In particular, estrogens preserve skeletal integrity stimulating OB differentiation and OC apoptosis, while their deficiency increases the rate of osteocyte death, causing bone fragility [26–28]. In women at the menopause, the significant fall in circulating estrogens, alters bone remodeling with increased loss of bone mass and strength. Estrogens are critical for the maintenance of normal bone structure also in men, where their decline accelerates bone turnover and osteopaenia [29]. The estrogens can directly influence immune system response inhibiting the secretion of proinflammatory cytokines, including IL-6 and TNFα from monocytes and repressing Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB) transcriptional activity [30]. Estrogen deprivation leads to dramatic elevations in the number of basic multicellular units (BMUs) that increase cortical porosity and extend the resorption area on trabecular surfaces. This phenomenon is due to a complex interplay of estrogens and cytokines that converge to an increase of OC lifespan and recruitment to bone surfaces [31,32]. Moreover, the increase in new bone deposition induced by estrogen deficiency that is accompanied by an augmentation in OB apoptosis is inadequate to compensate the enhanced bone resorption [33]. In addition, the elevated production of inflammatory cytokines, following estrogen deprivation, rises the apoptotic rate of mature OB limiting their activity [34,35].