ArticleCell death & disease2021
Age-related accumulation of advanced oxidation protein products promotes osteoclastogenesis through disruption of redox homeostasis.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Intelligent responsive alloy scaffold temporally regulates the immune-osteogenic axis for the treatment of infectious bone defects.Bioactive materials · 2026Article
- Friedelin Enhances Gelatin/Nanohydroxyapatite Scaffold Performance by Inhibiting Osteoclastogenesis and Promoting Osteogenesis.ACS omega · 2026Article
- Protein oxidation in crowded environments.The Biochemical journal · 2026Review
- Genetic and pharmacologic modulation of RAGE rescues the diabetes-mediated impairments to bone at multiple length scales.bioRxiv : the preprint server for biology · 2026Article
- Elastin-derived extracellular matrix fragments drive aging through innate immune activation.Nature aging · 2025Article
- Exercise suppresses osteoclastogenesis by increasing the secretion of muscle-derived L-β-aminoisobutyric acid.Journal of sport and health science · 2025Article
- Accumulation of advanced oxidation protein products aggravates bone-fat imbalance during skeletal aging.Journal of orthopaedic translation · 2025Article
- Association of dietary niacin intake with osteoporosis in the postmenopausal women in the US: NHANES 2007-2018.Frontiers in medicine · 2025Article
- AQP1 differentially orchestrates endothelial cell senescence.Redox biology · 2024Article
- Berberine attenuates brain aging via stabilizing redox homeostasis and inflammation in an accelerated senescence model of Wistar rats.Metabolic brain disease · 2024Article
- Older Tissue Age Derived From Abdominal Computed Tomography Biomarkers of Muscle, Fat, and Bone Is Associated With Chronic Conditions and Higher Mortality.Mayo Clinic proceedings · 2024Article
- Osteoclasts and osteoarthritis: Novel intervention targets and therapeutic potentials during aging.Aging cell · 2024Review
- Age-related decline in melatonin contributes to enhanced osteoclastogenesis via disruption of redox homeostasis.Molecular medicine (Cambridge, Mass.) · 2024Article
- Glycobiology in osteoclast differentiation and function.Bone research · 2023Review
- Exosome Release Delays Senescence by Disposing of Obsolete Biomolecules.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Crosstalk Between Senescent Bone Cells and the Bone Tissue Microenvironment Influences Bone Fragility During Chronological Age and in Diabetes.Frontiers in physiology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enhanced osteoclastogenesis is one of the major causes of age-related bone loss. Aging is accompanied by accumulation of advanced oxidation protein products (AOPPs). However, whether AOPPs accumulation contributing to the osteoclastogenesis with aging remains unclear. Here, we showed that AOPPs accumulation was associated with the enhanced osteoclastogenesis and deterioration of bone microstructure in aged mice. In vitro, AOPPs directly induced osteoclastogenesis by interaction with receptor activator of nuclear factor κ B (RANK) and the receptor for advanced glycation end products (RAGE) in the primary bone marrow monocytes. Bindings of AOPPs to RANK and RAGE were able to activate nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, trigger generation of reactive oxygen species, then induce phosphorylation of mitogen-activated protein kinases and c-fos, upregulation of the nuclear factor of activated T cell c1, eventually induce bone marrow monocytes to differentiate into mature osteoclasts. Chronic exposure to AOPPs enhanced osteoclastogenesis and bone loss in mice, which could be alleviated by NADPH oxidase inhibitor apocynin. Local injection of AOPPs into subperiosteal area induced bone resorption at the site of administration, which was similar to the effect of RANK ligand. Together, these results suggested that AOPPs could serve as a novel regulator of osteoclastogenesis and AOPPs accumulation might play an important role in the development of age-related bone loss.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.