ArticleThe Journal of biological chemistry2015
p47phox-Nox2-dependent ROS Signaling Inhibits Early Bone Development in Mice but Protects against Skeletal Aging.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- Evaluation of the effect of tartrazine on the offspring rats in an in vivo experimental model.Food science & nutrition · 2024Article
- Nox4 expression in osteo-progenitors controls bone development in mice during early life.Communications biology · 2022Article
- Estrogen prevents cellular senescence and bone loss through Usp10-dependent p53 degradation in osteocytes and osteoblasts: the role of estrogen in bone cell senescence.Cell and tissue research · 2021Article
- Review
- [Role of p22phox and NOX5 in autophagy and apoptosis of osteoblasts induced by hypoxia].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2021Article
- Short-Term Increased Physical Activity During Early Life Affects High-Fat Diet-Induced Bone Loss in Young Adult Mice.JBMR plus · 2021Article
- Nox4 Expression Is Not Required for OVX-Induced Osteoblast Senescence and Bone Loss in Mice.JBMR plus · 2020Article
- Induction of HO-1 by Mevastatin Mediated via a Nox/ROS-Dependent c-Src/PDGFRα/PI3K/Akt/Nrf2/ARE Cascade Suppresses TNF-α-Induced Lung Inflammation.Journal of clinical medicine · 2020Article
- NADPH Oxidase 2-Mediated Insult in the Auditory Cortex of Zucker Diabetic Fatty Rats.Neural plasticity · 2019Article
- Redox Signaling of NADPH Oxidases Regulates Oxidative Stress Responses, Immunity and Aging.Antioxidants (Basel, Switzerland) · 2018Review
- Article
- Microtubules tune mechanotransduction through NOX2 and TRPV4 to decrease sclerostin abundance in osteocytes.Science signaling · 2017Article
- NADPH oxidase-mediated redox signaling promotes oxidative stress resistance and longevity througheLife · 2017Article
- Ncf1 affects osteoclast formation but is not critical for postmenopausal bone loss.BMC musculoskeletal disorders · 2016Article
- Reactive Oxygen Species Differentially Regulate Bone Turnover in an Age-Specific Manner in Catalase Transgenic Female Mice.The Journal of pharmacology and experimental therapeutics · 2016Article
- Annexin A2 Modulates ROS and Impacts Inflammatory Response via IL-17 Signaling in Polymicrobial Sepsis Mice.PLoS pathogens · 2016Article
- Deciphering the Potential Pharmaceutical Mechanism of Chinese Traditional Medicine (Gui-Zhi-Shao-Yao-Zhi-Mu) on Rheumatoid Arthritis.Scientific reports · 2016Observational
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Bone remodeling is age-dependently regulated and changes dramatically during the course of development. Progressive accumulation of reactive oxygen species (ROS) has been suspected to be the leading cause of many inflammatory and degenerative diseases, as well as an important factor underlying many effects of aging. In contrast, how reduced ROS signaling regulates inflammation and remodeling in bone remains unknown. Here, we utilized a p47(phox) knock-out mouse model, in which an essential cytosolic co-activator of Nox2 is lost, to characterize bone metabolism at 6 weeks and 2 years of age. Compared with their age-matched wild type controls, loss of Nox2 function in p47(phox-/-) mice resulted in age-related switch of bone mass and strength. Differences in bone mass were associated with increased bone formation in 6-week-old p47(phox-/-) mice but decreased in 2-year-old p47(phox-/-) mice. Despite decreases in ROS generation in bone marrow cells and p47(phox)-Nox2 signaling in osteoblastic cells, 2-year-old p47(phox-/-) mice showed increased senescence-associated secretory phenotype in bone compared with their wild type controls. These in vivo findings were mechanistically recapitulated in ex vivo cell culture of primary fetal calvarial cells from p47(phox-/-) mice. These cells showed accelerated cell senescence pathway accompanied by increased inflammation. These data indicate that the observed age-related switch of bone mass in p47(phox)-deficient mice occurs through an increased inflammatory milieu in bone and that p47(phox)-Nox2-dependent physiological ROS signaling suppresses inflammation in aging.
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