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ROS production has long been linked to bone remodeling [12], but excessive ROS due to either estrogen deficiency [13], a lack of antioxidants in the diet [14], or secondary to other diseases can disrupt normal bone remodeling and lead to osteoclastogenesis [15]

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GSEA analysis further revealed significant enrichment of a tenascin-C-induced gene signature

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multiple mono-ubiquitination, in which multiple lysine residues of a substrate protein are tagged by several mono-ubiquitin molecules at the same time