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Mechano-transduction in Osteoblastic Cells involves Strain-regulated Estrogen Receptor -mediated Control of Insulin-like Growth Factor (IGF) I Receptor Sensitivity to Ambient IGF, Leading to Phosphatidylinositol 3-Kinase/AKT-dependent Wnt/LRP5 Receptor-

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TLDR
An initial cascade of strain-related events in osteoblasts is suggested in which strain activates IGF-IR, in association with ERα, so initiating phosphatidylinositol 3-kinase/AKT-dependent activation of β-catenin and altered lymphoid-enhancing factor/T cell factor transcription.
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The article was published on 2010-01-01 and is currently open access. It has received 106 citations till now. The article focuses on the topics: Growth factor receptor & Estrogen receptor beta.

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Estrogens and Androgens in Skeletal Physiology and Pathophysiology.

TL;DR: A comprehensive review of the molecular and cellular mechanisms of action of estrogens and androgens on bone, their influences on skeletal homeostasis during growth and adulthood, the pathogenetic mechanisms of the adverse effects of their deficiency on the female and male skeleton, as well as the role of natural and synthetic estrogenic or androgenic compounds in the pharmacotherapy of osteoporosis is provided.
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Mechanical regulation of signaling pathways in bone.

TL;DR: An understanding of mechanical regulation of bone signaling is crucial to understanding bone physiology, the etiology of diseases such as osteoporosis, and to the development of interventions to improve bone strength.
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Muscle and bone, two interconnected tissues

TL;DR: The understanding of this system will enable to define new levers to prevent/treat sarcopenia and osteoporosis at the same time, which might include nutritional interventions and physical exercise.
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Sex Steroid Actions in Male Bone

TL;DR: It is proposed that estrogens influence fracture risk in aging men via direct effects on bone, whereas androgens exert an additional antifracture effect mainly via extraskeletal parameters such as muscle mass and propensity to fall.

Osteocyte-Driven Bone Remodeling

TL;DR: Osteocytes, the most abundant cells in bone, have been long postulated to detect and respond to mechanical and hormonal stimuli and to coordinate the function of osteoblasts and osteoclasts as mentioned in this paper.
References
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AKT/PKB signaling: navigating downstream.

TL;DR: Those Akt substrates that are most likely to contribute to the diverse cellular roles of Akt, which include cell survival, growth, proliferation, angiogenesis, metabolism, and migration are discussed.
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New insights into tumor suppression: PTEN suppresses tumor formation by restraining the phosphoinositide 3-kinase/AKT pathway

TL;DR: A series of publications over the past year now suggest a mechanism by which PTEN loss of function results in tumors, and PTEN appears to negatively control the phosphoinositide 3-kinase signaling pathway for regulation of cell growth and survival by dephosphorylating the 3 position ofosphoinositides.
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Mechanical stimulation of bone in vivo reduces osteocyte expression of Sost/sclerostin

TL;DR: Modulation of sclerostin levels appears to be a finely tuned mechanism by which osteocytes coordinate regional and local osteogenesis in response to increased mechanical stimulation, perhaps via releasing the local inhibition of Wnt/Lrp5 signaling.
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