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The ERS inducer TG increased osteoclastogenesis through RANKL-induced NF-B activation and ROS production, while IL-1 promoted RANKL-mediated osteoclast formation by upregulating GRP78, PERK, and IRE1
The dysregulation of T cell glucose metabolism, especially the pathological reprogramming towards a hyperglycolytic phenotype, has emerged as a critical focus in understanding RA pathogenesis
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The ability of SP-A to inhibit bacterial growth and macrophage phagocytosis in vitro was attenuated due to its conformational changes
