Results 11 to 20 of about 11,099 (162)

Cortical bone adaptation to a moderate level of mechanical loading in male Sost deficient mice

open access: yesScientific Reports, 2020
Loss-of-function mutations in the Sost gene lead to high bone mass phenotypes. Pharmacological inhibition of Sost/sclerostin provides a new drug strategy for treating osteoporosis.
Haisheng Yang   +10 more
doaj   +4 more sources

SOST Inhibits Prostate Cancer Invasion. [PDF]

open access: yesPLoS ONE, 2015
Inhibitors of Wnt signaling have been shown to be involved in prostate cancer (PC) metastasis; however the role of Sclerostin (Sost) has not yet been explored.
Bryan D Hudson   +8 more
doaj   +3 more sources

Lipid Nanoparticle Delivery of siRNA to Osteocytes Leads to Effective Silencing of SOST and Inhibition of Sclerostin In Vivo

open access: yesMolecular Therapy: Nucleic Acids, 2016
Sclerostin is a protein secreted by osteocytes that is encoded by the SOST gene; it decreases bone formation by reducing osteoblast differentiation through inhibition of the Wnt signaling pathway.
Genc Basha   +6 more
doaj   +2 more sources

Expression of Sclerostin in Osteoporotic Fracture Patients Is Associated with DNA Methylation in the CpG Island of the SOST Gene

open access: yesInternational Journal of Genomics, 2019
Purpose. SOST gene is one of the key factors in regulating bone absorption. Although there are reports showing diverse transcription factors, epigenetic modification could be responsible for regulating SOST gene expression.
Yanming Cao   +10 more
doaj   +2 more sources

Heterozygous deletion of both sclerostin (Sost) and connexin43 (Gja1) genes in mice is not sufficient to impair cortical bone modeling. [PDF]

open access: yesPLoS ONE, 2017
Connexin43 (Cx43) is the main gap junction protein expressed in bone forming cells, where it modulates peak bone mass acquisition and cortical modeling.
Susan K Grimston   +3 more
doaj   +2 more sources

Piezo1 Activation Rescues Anabolic Response to Mechanical Loading in Aged Bone via Connexin 43 Hemichannels. [PDF]

open access: yesAging Cell
Yoda1‐induced Piezo1 activation enhances Piezo1‐Cx43 interaction upon mechanical stimulation, triggering PI3K‐Akt signaling to drive Cx43 phosphorylation and hemichannel opening. These events elevate PGE2 release, suppress SOST expression in senescent osteocytes, and ultimately enhance bone anabolism on the endosteal surface.
Zhao D   +10 more
europepmc   +2 more sources

Characterising skull pathologies in the Sost-deficient mouse for preclinical evaluation of sclerosteosis treatments. [PDF]

open access: yesDis Model Mech
Facial paralysis, hearing loss and potentially lethal raised intracranial pressure are primary symptoms of sclerosteosis, an ultra-rare, autosomal recessive high bone mass (HBM) condition that predominantly manifests in skull pathologies.
Dreyer TJ   +6 more
europepmc   +2 more sources

Quantification of the Tissue Sodium Concentration in the Human Calf at 7T With Reduced Acquisition Time: Influence of the Nominal Spatial Resolution. [PDF]

open access: yesNMR Biomed
Fast 23Na MRI of the human calf at 7T was achieved by reducing nominal spatial resolution. Shorter measurement times can improve clinical feasibility of 23Na MRI while preserving reliable quantification of apparent tissue sodium concentration through partial volume, relaxation, and B0/B1 corrections.
Höhn JM   +6 more
europepmc   +2 more sources

Sclerostin Suppression Facilitates Uveal Melanoma Progression Through Activating Wnt/β-Catenin Signaling Via Binding to Membrane Receptors LRP5/LRP6

open access: yesFrontiers in Oncology, 2022
ObjectiveUveal melanoma (UM) is the most frequent primary eye cancer in adults with a 50% mortality rate. Characterizing the fundamental signaling pathways that drive UM is of importance for the development of targeted therapy.
Hanqing Wang   +9 more
doaj   +1 more source

Epigenetic Regulation of Bone Homeostasis in Osteoporosis: Mechanisms, Evidence Gaps, and Translational Prospects. [PDF]

open access: yesCell Biochem Funct
ABSTRACT Osteoporosis arises from an imbalance among osteoblast‐mediated bone formation, osteoclast‐mediated bone resorption, and osteocyte‐directed mechanosensory control, but the molecular events that connect aging, hormonal change, inflammation, and mechanical unloading to bone loss remain incompletely resolved.
Du M, Wang L.
europepmc   +2 more sources

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