Bone Metabolism and Diseases

This study investigates the osteoprotective effects of Skeletonema costatum extract by modulating immune pathways in zebrafish and medaka models, showing inhibition of osteoclast differentiation and bone loss.

This study shows shear stress inhibits adipocyte differentiation by downregulating lncRNA MALAT1 in mesenchymal stem cells, linking mechanical cues to lncRNA regulation in bone remodeling.

This study generates an Fzd8-knockout mouse model using CRISPR/Cas9 to investigate its role in bone development and homeostasis, finding altered osteoclast and osteoblast activity and potential links to osteoporosis.

This study shows NPC1L1 inhibits osteogenesis and promotes osteoporosis by regulating cholesterol metabolism through the C/EBP/Cyp27a1/27-OHC axis.

This study finds that inflammation in bone of T2D and obesity patients is linked to reduced Wnt signaling and lower bone strength.

This study identifies CD11B+CD36+ macrophages as bone anabolic cells that limit age-related cortical bone loss in mice and humans.

This study shows Osterix maintains osteocytic dendrites and intercellular communication by regulating Connexin43, impacting bone homeostasis and disease.

This study shows that Piezo1 on preosteoclasts reduces osteoclast formation and bone resorption in periodontitis via the PP2A-Akt pathway.

This paper identifies TAM receptors MERTK and TYRO3 in osteoclasts regulating bone homeostasis through RHOA-COFILIN-MYOSIN II signaling, with MERTK promoting osteoclast formation and TYRO3 inhibiting it.

The paper identifies KLF16 as an inhibitory regulator of osteogenic differentiation through transcriptomic analysis of human iPSC-derived cells and in vivo validation.

This study shows that loss of Cotl1 in mice reduces platelet-mediated osteoclastogenesis, leading to osteopetrosis, and identifies a genetic association between COTL1 variants and bone density in humans.

This paper identifies CCN3 as a brain-derived hormone that promotes bone mass in lactating females by compensating for estrogen loss and supporting skeletal stem cells.

This study generates Irf8 knock-in mice modeling the human IRF8G388S mutation, showing increased osteoclast activity and tooth root resorption while sparing immune cell development.

This study shows that YBX1 promotes bone formation through m5C-dependent regulation of CD31, EMCN, and BMP4 in endothelial cells, offering a therapeutic target for osteoporosis.

This study shows that vinculin inhibits Mef2c-driven sclerostin expression in osteocytes, promoting bone formation in mice by enhancing estrogen regulation.

This study identifies ATP6AP2 and MMP14 as critical for osteoblast-to-osteocyte transition, showing their role in osteocyte maturation, morphology, and bone matrix remodeling.

This study shows osteoclasts contribute to pain in arthritis by affecting bone vascularization and innervation, and inhibitors can reverse this pain.

This study shows that Ezh2 deletion in macrophages reduces osteoclastogenesis and increases bone mass in mice, suggesting an epigenetic role in bone remodeling.

This study shows that a PDGFRβ mutation causes skeletal stem cell defects leading to osteopenia and overgrowth in mice by altering osteogenic and chondrogenic pathways.

This study shows that Seliciclib promotes osteoblastic differentiation by enhancing F-actin and suppresses osteosarcoma cell migration.

The paper investigates how mitochondrial activation occurs during osteogenic differentiation and identifies Akt-dependent mechanisms and factors like Wnt3a and BMP2 that drive this process.

This study identifies miR-146a as a key regulator of age-related bone loss, showing its role in controlling bone homeostasis through Wnt signaling and its potential as a therapeutic target.

This study identifies a GABAergic neural circuit from the forebrain to hypothalamus that regulates anxiety-induced bone loss.

This study shows MACF1 is essential for bone formation by enabling SMAD7 nuclear translocation in MSCs, leading to ossification retardation and bone loss in mice.

This study shows that Osteocrin promotes both endochondral and intramembranous ossification in long bone growth by enhancing CNP signaling.

The paper reports a novel nonsense mutation in XLas causing osteopetrosis and high bone mass by disrupting the skeletal response to parathyroid hormone.