Results 21 to 30 of about 13,466 (213)

In silico identification of sclerostin inhibitors

open access: yesMolecular Diversity
Wnt/β-catenin signaling pathway plays a major role in the regulation of bone homeostasis. Sclerostin exhibits a high-affinity binding to the Wnt co-receptors LRP5/6 and therefore acts as an extracellular inhibitor of canonical Wnt signaling. Disruption of the interaction between LRP5/6 and sclerostin is essential for Wnt-related metabolic processes ...
Sepici Dinçel, Aylin   +5 more
openaire   +4 more sources

Sclerostin is upregulated in the early stage of chondrogenic differentiation, but not required in endochondral ossification in vitro. [PDF]

open access: yesPLoS ONE, 2018
Sclerostin is a potent inhibitor of the canonical Wnt signaling pathway. Wnt signaling pathways have multiple roles in the regulation of cartilage development, growth, and maintenance.
Yasuteru Yamaguchi   +4 more
doaj   +1 more source

Disparate bone anabolic cues activate bone formation by regulating the rapid lysosomal degradation of sclerostin protein

open access: yeseLife, 2021
The downregulation of sclerostin in osteocytes mediates bone formation in response to mechanical cues and parathyroid hormone (PTH). To date, the regulation of sclerostin has been attributed exclusively to the transcriptional downregulation of the Sost ...
Nicole R Gould   +11 more
doaj   +1 more source

Does oxidative status affect serum sclerostin levels in patients with type 2 diabetes mellitus? [PDF]

open access: yesFolia Medica, 2023
Introduction: Sclerostin is a glycoprotein known as a negative regulator of bone formation, predominantly expressed by mature  osteocytes.
Ilhan Sabancilar   +4 more
doaj   +3 more sources

Inhibitors of sclerostin [PDF]

open access: yesCurrent Opinion in Rheumatology, 2014
Recent data suggest that inhibitors of sclerostin, an osteocyte-produced Wnt signaling pathway antagonist, can stimulate bone formation. This review provides rationale and summarizes recent evidence supporting this novel approach to skeletal anabolism.Data from numerous preclinical models in rodents and monkeys consistently demonstrate that ...
Matthew T, Drake, Joshua N, Farr
openaire   +2 more sources

Serum sclerostin levels in osteoporotic fracture patients [PDF]

open access: yes, 2022
PURPOSE: Sclerostin inhibits bone formation and stimulates bone resorption. Previous studies found a positive association between bone density and serum sclerostin, but literature on sclerostin levels in osteoporotic fracture patients is scarce.
Krijnen, Pieta   +9 more
core   +1 more source

Osteocyte TSC1 promotes sclerostin secretion to restrain osteogenesis in mice [PDF]

open access: yesOpen Biology, 2019
Osteocytes secrete the glycoprotein sclerostin to inhibit bone formation by osteoblasts, but how sclerostin production is regulated in osteocytes remains unclear.
Wen Liu   +14 more
doaj   +1 more source

Endocrine functions of sclerostin

open access: yesCurrent Opinion in Endocrine and Metabolic Research, 2023
Sclerostin, the product of the SOST gene has primarily been studied for its profound impact on bone mass. By interacting with LRP5 and LRP6, the glycoprotein suppresses the propagation of Wnt signals to β-catenin and thereby suppresses new bone formation.
openaire   +2 more sources

Sclerostin regulation: a promising therapy for periodontitis by modulating alveolar bone

open access: yesChinese Medical Journal, 2020
. Periodontitis is one of the most prevalent epidemics affecting human health and life recently, and exploration of the pathogenesis and treatment of periodontitis has been valued by scholars.
Tian-Jiao Li   +5 more
doaj   +1 more source

Cardioprotective function of sclerostin by reducing calcium deposition, proliferation, and apoptosis in human vascular smooth muscle cells

open access: yesCardiovascular Diabetology, 2023
Background Sclerostin is an inhibitor of the Wnt/b-catenin pathway, which regulates bone formation, and can be expressed in vascular smooth muscle cells (VSMCs).
Sheila González-Salvatierra   +9 more
doaj   +1 more source

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