Objective: This study investigates NOX4, an enzyme producing hydrogen peroxide, in endochondral ossification and bone remodeling. NOX4’s role in osteoblast formation and osteogenic signaling pathways is explored. Methods: Using NOX4-deficient (NOX4−/− ) and ovariectomized (OVX) mice, we identify NOX4’s potential mediators in bone maturation. Results: NOX4−/− mice displayed significant differences in bone mass and structure.Compared to the normal Control and OVX groups. Hematoxylin and eosin staining showed NOX4−/− mice had the highest trabecular bone volume, while OVX had the lowest. Proteomic analysis revealed significantly elevated MPO and OPN levels in bone marrow-derived cells in NOX4−/− mice. Immunohistochemistry confirmed increased MPO, OPN, and collagen II (COLII) near the epiphyseal plate. Collagen and chondrogenesis analysis supported enhanced bone development in NOX4−/− mice. Conclusions and Relevance: Our results emphasize NOX4’s significance in bone morphology, mesenchymal stem cell proteomics, immunohistochemistry, collagen levels, and chondrogenesis. NOX4 deficiency enhances bone development and endochondral ossification, potentially through increased MPO, OPN, and COLII expression. These findings suggest therapeutic implications for skeletal disorders.

Objective: This study investigates NOX4, an enzyme producing hydrogen peroxide, in endochondral ossification and bone remodeling. NOX4’s role in osteoblast formation and osteogenic signaling pathways is explored. Methods: Using NOX4-deficient (NOX4−/− ) and ovariectomized (OVX) mice, we identify NOX4’s potential mediators in bone maturation. Results: NOX4−/− mice displayed significant differences in bone mass and structure.Compared to the normal Control and OVX groups. Hematoxylin and eosin staining showed NOX4−/− mice had the highest trabecular bone volume, while OVX had the lowest. Proteomic analysis revealed significantly elevated MPO and OPN levels in bone marrow-derived cells in NOX4−/− mice. Immunohistochemistry confirmed increased MPO, OPN, and collagen II (COLII) near the epiphyseal plate. Collagen and chondrogenesis analysis supported enhanced bone development in NOX4−/− mice. Conclusions and Relevance: Our results emphasize NOX4’s significance in bone morphology, mesenchymal stem cell proteomics, immunohistochemistry, collagen levels, and chondrogenesis. NOX4 deficiency enhances bone development and endochondral ossification, potentially through increased MPO, OPN, and COLII expression. These findings suggest therapeutic implications for skeletal disorders.

Objective: This study investigates NOX4, an enzyme producing hydrogen peroxide, in endochondral ossification and bone remodeling. NOX4’s role in osteoblast formation and osteogenic signaling pathways is explored. Methods: Using NOX4-deficient (NOX4−/− ) and ovariectomized (OVX) mice, we identify NOX4’s potential mediators in bone maturation. Results: NOX4−/− mice displayed significant differences in bone mass and structure.Compared to the normal Control and OVX groups. Hematoxylin and eosin staining showed NOX4−/− mice had the highest trabecular bone volume, while OVX had the lowest. Proteomic analysis revealed significantly elevated MPO and OPN levels in bone marrow-derived cells in NOX4−/− mice. Immunohistochemistry confirmed increased MPO, OPN, and collagen II (COLII) near the epiphyseal plate. Collagen and chondrogenesis analysis supported enhanced bone development in NOX4−/− mice. Conclusions and Relevance: Our results emphasize NOX4’s significance in bone morphology, mesenchymal stem cell proteomics, immunohistochemistry, collagen levels, and chondrogenesis. NOX4 deficiency enhances bone development and endochondral ossification, potentially through increased MPO, OPN, and COLII expression. These findings suggest therapeutic implications for skeletal disorders.

Objective: This study investigates NOX4, an enzyme producing hydrogen peroxide, in endochondral ossification and bone remodeling. NOX4’s role in osteoblast formation and osteogenic signaling pathways is explored. Methods: Using NOX4-deficient (NOX4−/− ) and ovariectomized (OVX) mice, we identify NOX4’s potential mediators in bone maturation. Results: NOX4−/− mice displayed significant differences in bone mass and structure.Compared to the normal Control and OVX groups. Hematoxylin and eosin staining showed NOX4−/− mice had the highest trabecular bone volume, while OVX had the lowest. Proteomic analysis revealed significantly elevated MPO and OPN levels in bone marrow-derived cells in NOX4−/− mice. Immunohistochemistry confirmed increased MPO, OPN, and collagen II (COLII) near the epiphyseal plate. Collagen and chondrogenesis analysis supported enhanced bone development in NOX4−/− mice. Conclusions and Relevance: Our results emphasize NOX4’s significance in bone morphology, mesenchymal stem cell proteomics, immunohistochemistry, collagen levels, and chondrogenesis. NOX4 deficiency enhances bone development and endochondral ossification, potentially through increased MPO, OPN, and COLII expression. These findings suggest therapeutic implications for skeletal disorders.