Figure 1 from FoxO1/NLRP3 Inflammasome Promotes Age-Related Alveolar Bone Resorption | Semantic Scholar (2024)

FoxO1 knockdown contributed to the inhibition of osteoclastogenesis by effectively suppressing NF-κB signaling and NLRP3 inflammasome activation and provides a viable therapeutic target for periodontitis treatment.

This special issue encompasses a collection of articles dedicated to recent advances in the behavioral and social implications of age-related oral diseases and tooth loss on several aspects of the quality of life of adults as they age.

A summary of NLRP3 inflammasome activation and its impact on OBs is provided and the significant roles of NLRP3 inflammasome in regulating OBs differentiation and function are highlighted.

How the FOXO1 signaling axis can regulate periodontal bacteria-epithelial interactions, immune-inflammatory response, bone remodeling, and wound healing is summarized.

It is shown that intracellular H2O2 accumulation is a critical and purposeful adaptation for the differentiation and survival of osteoclasts, the bone cells responsible for the resorption of mineralized bone matrix, using mice with conditional loss or gain of FoxO transcription factor function.

It is demonstrated that the NLRP3 inflammasome plays a vital role in the pathogenesis of osteoporosis by affecting the differentiation of osteoblasts and osteoclasts, and overall not only accelerates bone resorption, but also inhibits bone formation, thus increasing the risk of bone formation.

It is found that an increased level of reactive oxygen species with aging stimulates the expression of miR-218, which directly targets Rictor and reduces osteoblast bone surface adhesion and survival, resulting in a decreased number of functional osteoblasts and accelerated bone loss in aged mice.

In vitro studies suggest that reduced DC numbers in lymph nodes of aged mice may involve the effect of advanced glycation end products on DC migration, and the greater adaptive immune response in aged versus young mice was linked to enhanced levels of P. gingivalis and reduced bacterial diversity.

Diversion of the limited pool of β-catenin from T-cell factor- to FoxO-mediated transcription in osteoblastic cells may account, at least in part, for the attenuation of osteoblastogenesis and bone formation by the age-dependent increase in oxidative stress.

FoxO1 in osteoblasts uses a previously unrecognized mechanism to preserve redox balance by promoting protein synthesis and subsequently inhibiting cell cycle arrest, which indicates that FoxO1 integrates and orchestrates responses to different stress signals to maintain bone cell function and preserve skeletal homeostasis.

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