Kelly B Emerton's research while affiliated with Icahn School of Medicine at Mount Sinai and other places

... Some studies have reported a higher rate of osteocyte death in the bones of mice and patients with postmenopausal osteoporosis, which is caused in part by the loss of the osteoprotective effects of estrogen (ref. [31][32][33]. Excessive osteocyte death disrupts the balance between bone formation and absorption, leading to PMOP (ref. 4). ...

... Ovariectomy induces periosteal bone growth in the diaphysis of long bones and cortical bone of the mid-shaft [36]. Conversely, the ovariectomized rat demonstrates enhanced degeneration of bones in the mid-diaphyseal, endosteum, resulting in a broadening of the medullary cavity [37,38]. ...

... The proliferation and differentiation of growth plate chondrocytes are regulated by extrinsic factors such as GH-IGF-I, glucocorticoids, and estrogen (Shim et al., 2015;Karimian et al., 2012;Shantanam et al., 2018). Previous research indicates that reduced expression of Igf-I/Igfbp3/Igfals in the liver leads to impaired chondrocyte proliferation and shorter femur length, emphasizing the importance of these factors in postnatal bone development (Yakar et al., 2002 ;Yakar et al., 2009 ). As the IGF pathway proteins are downregulated in whole-body SMA mice, the bone growth defects observed in the mice have sparked debate as it remains unclear whether they are due to intrinsic factors, such as chondrocyte SMN reduction, or the low IGF axis level (Hua et al., 2011 ;Tsai et al., 2014 ;Deguise et al., 2021 ;Hensel et al., 2015). ...