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Elucidation of estrogen receptor function in bone with the use of mouse models
Sara H Windahl1, Göran Andersson, Jan-Ake Gustafsson
1Dept Biosciences, Karolinska Institutet, Novum, Huddinge, SE-14157, Sweden.
Abstract:
Since the discovery that estrogen receptors (ERs) are present in bone cells, there has been intense research into the action of estrogen in bone. During the past decade, humans with disturbed estrogen signaling, either as a result of ER alpha or aromatase deficiency, have been reported. Furthermore, mouse models have been established with a deficiency of ER alpha, ER beta or both, in addition to deficiency of aromatase. This review focuses on data accumulated during the past three years from studies of knockout mice with impaired estrogen signaling resulting from ER or aromatase deficiency.
Insights
Estrogen receptors (ERs) and aromatase are crucial for bone health. Studies on knockout mice with impaired estrogen signaling reveal new insights into estrogen
Area of Science:
- Bone biology
- Endocrinology
- Genetics
Background:
- Estrogen receptors (ERs) are present in bone cells, prompting extensive research into estrogen's role in bone.
- Human studies have identified individuals with disrupted estrogen signaling due to ER alpha or aromatase deficiency.
- Mouse models with deficiencies in ER alpha, ER beta, or aromatase have been developed to study these effects.
Purpose of the Study:
- To review recent findings on the role of estrogen signaling in bone health.
- To focus on data from the past three years concerning estrogen's effects on bone.
- To analyze studies involving knockout mice with impaired estrogen signaling.
Main Methods:
- Review of scientific literature published in the last three years.
- Analysis of data from knockout mouse models with deficiencies in estrogen signaling pathways.
- Focus on models with impaired ER alpha, ER beta, or aromatase function.
Main Results:
- Recent studies highlight the critical role of estrogen signaling in maintaining bone density and integrity.
- Impaired estrogen signaling, whether through ER or aromatase deficiency, leads to significant bone abnormalities.
- Knockout mouse models provide valuable insights into the specific functions of ER alpha and ER beta in bone.
Conclusions:
- Estrogen signaling is essential for normal bone metabolism and homeostasis.
- Targeting estrogen pathways presents potential therapeutic strategies for bone diseases.
- Further research in genetically modified models will continue to elucidate complex estrogen-bone interactions.