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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.
Potential of paracetamol for reproductive disruption: molecular interaction, dynamics, and MM-PBSA based in-silico assessment
Published in Toxicology Mechanisms and Methods, 2023
Sayed Aliul Hasan Abdi, Abuzer Ali, Shabihul Fatma Sayed, Amena Ali, Shaivad Shabee Hulhasan Abadi, Abu Tahir, Mohd Amir Afjal, Hina Rashid, Omar M. Aly, Sumathi Nagarajan
Estrogen receptor beta (ERβ) is also activated by sex hormone (Antal et al. 2012). Irrational prescribing of paracetamol may disrupt ERβ also, regarding the stability of paracetamol with ERβ the RMSD exhibited that paracetamol was stable during MD simulation for a period of 10 ns, the RMSD attained equilibrium at ∼0.15 Å (range 0.05–0.05 nm) for paracetamol, bisphenol and for tamoxifen (Figure 4(A)). Moreover, RMSF analysis exhibited that the 1QKM complex with paracetamol, bisphenol, and tamoxifen was in better stability (Figure 4(B)). The radius of gyration for 1QKM complex with paracetamol, bisphenol, and tamoxifen were fluctuated and decreased at 1.77–1.79, 1.76–1.78, and 1.77–1.79 nm, respectively (Figure 4(C)). The number of Hydrogen bonds after 10 ns was observed (Figure 4(D)). In addition, the SASA values for the 1QKM—paracetamol, 1QKM—bisphenol, 1QKM—tamoxifen were 15–18, 15–20, and 15–18 nm, respectively (Figure 4(E)). The motion capture by eigenvectors was 90% for paracetamol (Figures 5(A,B)), for bisphenol (Figures 5(C,D)) 93% for tamoxifen 90% (Figures 5(E,F)). Each dot represents one complex confirmation in the graph, which displays the variance in the conformational distribution.
High prevalence of autoimmune diseases in women with endometriosis: a case-control study
Published in Gynecological Endocrinology, 2020
M. G. Porpora, S. Scaramuzzino, C. Sangiuliano, I. Piacenti, V. Bonanni, M. G. Piccioni, R. Ostuni, L. Masciullo, P. L. Benedetti Panici
Humoral immunity can explain the correlation with autoimmune thyroid diseases. A higher reactivity of some autoantibodies (e.g. TPOAb) in patients with endometriosis has been found. Moreover, it seems that the incidence of positive ANAs is higher in patients with endometriosis as in patients with Graves’ disease. A further possible link between Graves’ disease and endometriosis is the estrogen effect: Graves’ disease is fivefold more prevalent among women than men. Estrogens are important modulators of the immune system as regulators of cytokine expression, antigen presentation, and B-cell lymphopoiesis. The exact effect of the estrogen receptor β on the function of the immune system is not clear but available data suggest that signaling through estrogen receptor beta gene (ESR2) may have a suppressive effect. Differential expression of the ESR2 was confirmed recently in patients with endometriosis. In addition, polymorphism of the ESR2 is associated with susceptibility to Graves’ disease. Thus, changes in ESR2 function might be a common link between Graves’ disease and endometriosis [27,33].
High serum concentration of estradiol may be a risk factor of prostate enlargement in aging male in China
Published in The Aging Male, 2020
Ding Xu, Yu Wu, Haibo Shen, Subo Qian, Jun Qi
In the estrogen pathway, estrogen receptors play an important role in modulating estrogen action. Estrogen action is mediated by two nuclear receptors: estrogen receptor-alpha (ERα) and estrogen receptor-beta (ERβ). ERα is a key mediator and putative therapeutic target for bladder complications of BPH. It has been reported that, while ERα is an oncogenic factor involved in cell proliferation and survival, ERβ is a protective factor that is anti-carcinogenic and pro-apoptotic. Recent experimental animal models on prostatic hyperplasia support estrogen receptors as critical factors in the prostatic hyperplastic response [29]. E2 has been shown to promote prostate proliferation through activating ERα [9] and cells expressing ERα were more prevalent in human BPH [30]. Moreover, Park et al. suggested that the mechanism of estrogen-regulated cell growth and the role of stromal cells may be different in normal versus BPH prostates. Normal stromal cells predominantly used rapid E2 signaling, but BPH stromal cells used classical ER-signaling, which was inhibited by treatment with ER antagonist [31]. To some extent, these may explain why the higher serum E2 level, the higher prostate volume in BPH patients.