HRT was associated with a decrease in iron stores in post-reproductive women in the absence of uterine blood loss, indicating a possible homeostatic hormonal control of iron status. The hormone estradiol can interfere with the way the body metabolizes iron. Many menopausal women may also have low levels even if they are not menstruating. In this potentially important study, the authors attempt to explain why estrogen hormone replacement therapy is not effective in preventing atherosclerosis in postmenopausal women, demonstrating that iron accumulation prevents hormone replacement therapy from benefiting by negatively regulating estrogen receptor expression through mediated proteolysis.
by MDM2. Currently, the strength of the evidence is incomplete, as control groups are lacking and there is no clear evidence that this effect is related to estradiol treatment as well as to iron accumulation in the postmenopausal state. This work may be of interest to the general public, as well as to specialists. During perimenopause, changes in estrogen levels can also affect the way the body manages iron (1). Estrogen helps the body absorb iron by reducing a hormone called hepcidin, which usually slows iron absorption.
When estrogen levels decrease, levels of hepcidin can increase, making it difficult for the body to absorb iron from food (1). This, combined with the heavy bleeding that is common during this period, can lead to iron deficiency, as the body depletes iron stores faster than it can replace them. This study suggests that immediate hormone replacement therapy after menopause, together with adequate iron chelation, may provide AD benefits. Hormone therapy is recommended immediately after menopause, along with adequate iron chelation to protect against atherosclerosis. Our objective was to investigate the impact of aging-related iron accumulation on the therapeutic effect of hormone replacement therapy on rheumatoid arthritis and to explore the underlying mechanisms.
This highlights the need for clinical studies that investigate how iron levels influence the benefits of hormone therapy for cardiovascular health after menopause. With the efficacy of hormone replacement therapy questioned by the “window of opportunity” theory (Yesufu et al., 200), it is vital to explore therapies that maintain ERα expression by mediating the protective effects of estrogen. While further work is needed to determine if iron restriction therapy is clinically relevant in combination with hormone replacement therapy for the intervention of postmenopausal atherosclerosis as a long-term strategy, this article provides guidelines for optimizing the timing of intervention with this therapy and supportive nutritional treatment. We wonder if aging-related iron accumulation affects estrogen receptor α (ERα) expression, which explains the ineffectiveness of hormone replacement therapy.
Therefore, iron and estradiol together downregulate ERα through MDM2-mediated proteolysis, which could explain TRH failures in late postmenopausal patients with aging-related iron accumulation. We asked if aging-related iron accumulation affects estrogen receptor α (ERα) expression, which explains the ineffectiveness of TRH. This study involved 20 postmenopausal patients (at least one year since menopause, without hormone replacement therapy) aged 54 to 84, recruited to the Department of Vascular Surgery of the Drum Tower Affiliated Hospital of the Faculty of Medicine of Nanjing University. In EPM, iron retention was mild and ERα responded to the application of TRH to achieve protective effects (A).
We propose that the combination of hormone replacement therapy and iron restriction therapy may be a long-term strategy to prevent the effects of E2 on the development of EA in postmenopausal women. Therefore, HRT is unlikely to result in an effective outcome in women with PMS as in women with PMS, unless combined with an iron chelation scheme. In summary, this study demonstrates the impact of iron overload on the proteolysis of ERα mediated by the enzyme E2 and its fundamental consequences on the outcome of hormone replacement therapy. However, the beneficial effect of hormone replacement therapy (HRT) is lost in late postmenopausal women with atherogenesis.
