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 ERα or aromatase deficiency, have been reported. Furthermore, mouse models have been established with a deficiency of ERα, ERβ 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.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism