Redox signaling and antioxidant defense in osteoclasts

Tao, Huaqiang; Li, Xuefeng; Wang, Qiufei; Yu, Lei; Yang, Peng; Chen, Wenlong; Yang, Xing; Zhou, Jun; Geng, Dechun

doi:10.1016/j.freeradbiomed.2023.12.043

Cited by 4 publications

(2 citation statements)

References 157 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A balanced redox capacity in mitochondria is required to maintain bone mass homeostasis; however, the loss of antioxidant function decreases bone-forming cell survival, reducing bone formation [69]. The overproduction of reactive oxygen radicals by aging or chronic inflammation promotes macrophage differentiation into osteoclastogenic lineages, increasing the bone resorption capacity and accelerating bone remodeling [70]. While oxidative stress is present in the development of age-or estrogen deficiency-mediated osteoporosis, which may be directly regulated through SOX9 [71], what the role the TCA cycle enzymes or intermediates may play in this feature warrants studies.…”

Section: The Tca Cycle Regulates Redox Homeostasismentioning

confidence: 99%

“…Among metabolites, acetyl-CoA and α-KG are an indispensable substrate and co-factor, respectively, for plenty of epigenetic regulators (Figure 2). lineages, increasing the bone resorption capacity and accelerating bone remodeling [70]. While oxidative stress is present in the development of age-or estrogen deficiency-mediated osteoporosis, which may be directly regulated through SOX9 [71], what the role the TCA cycle enzymes or intermediates may play in this feature warrants studies.…”

Section: Noncanonical Actions Of Tca Cycle Metabolism In Bone Formati...mentioning

confidence: 99%

See 1 more Smart Citation

Tricarboxylic Acid Cycle Regulation of Metabolic Program, Redox System, and Epigenetic Remodeling for Bone Health and Disease

Lian,

Wu,

Lin

et al. 2024

Antioxidants

View full text Add to dashboard Cite

Imbalanced osteogenic cell-mediated bone gain and osteoclastic remodeling accelerates the development of osteoporosis, which is the leading risk factor of disability in the elderly. Harmonizing the metabolic actions of bone-making cells and bone resorbing cells to the mineralized matrix network is required to maintain bone mass homeostasis. The tricarboxylic acid (TCA) cycle in mitochondria is a crucial process for cellular energy production and redox homeostasis. The canonical actions of TCA cycle enzymes and intermediates are indispensable in oxidative phosphorylation and adenosine triphosphate (ATP) biosynthesis for osteogenic differentiation and osteoclast formation. Knockout mouse models identify these enzymes’ roles in bone mass and microarchitecture. In the noncanonical processes, the metabolites as a co-factor or a substrate involve epigenetic modification, including histone acetyltransferases, DNA demethylases, RNA m6A demethylases, and histone demethylases, which affect genomic stability or chromatin accessibility for cell metabolism and bone formation and resorption. The genetic manipulation of these epigenetic regulators or TCA cycle intermediate supplementation compromises age, estrogen deficiency, or inflammation-induced bone mass loss and microstructure deterioration. This review sheds light on the metabolic functions of the TCA cycle in terms of bone integrity and highlights the crosstalk of the TCA cycle and redox and epigenetic pathways in skeletal tissue metabolism and the intermediates as treatment options for delaying osteoporosis.

show abstract

Section: The Tca Cycle Regulates Redox Homeostasismentioning

confidence: 99%

Section: Noncanonical Actions Of Tca Cycle Metabolism In Bone Formati...mentioning

confidence: 99%