Fig. 3.

ER stress in the pathogenesis of OP. a Bone remodeling is mainly regulated by the coupling of osteoblast-mediated bone formation and osteoclast-mediated bone resorption, and osteocytes have also been reported to participate in bone remodeling in OP. b RANKL activates CREBH through ROS/ER stress signaling pathway to promote the transcription of NFATc1, ultimately leading to increased osteoclastogenesis. c Autophagy deficiency induced by conditional Atg7 deletion inhibits mineralization and promotes ER stress and apoptosis in osteoblasts. CHOP C/EBP homologous protein, CREBH cAMP response element-binding protein H, C/EBPβ CCAAT/enhancer binding protein β, eIF2α α-subunit of eukaryotic translation initiation factor 2, ER endoplasmic reticulum, IRE1 inositol-requiring enzyme 1, MAPK8 mitogen-activated protein kinase 8, NFATc1 nuclear factor of activated T cells cytoplasmic 1, PERK protein kinase R-like ER kinase, RANKL receptor activator of NF-κB ligand, ROS reactive oxygen species, Runx2 Runt-related transcription factor 2, S1P site-1 membrane proteases, S2P site-2 membrane proteases, Smad small mother against decapentaplegic