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However, the mechanisms by which osteoclasts perceive and respond to mechanical disturbances remain unclear. Through integrating multi\u2010omics data of bone tissues from hindlimb unloading (HLU) and control mice, it is revealed that glutamine (Gln) catabolism\u2010induced suppression of apoptosis is critical for monocytes sensing and responding to mechanical unloading. Gln uptake is essential for the survival of monocytes under mechanical unloading. Deprivation of Gln or blockade of Gln transporter solute carrier family 1 member 5 (SLC1A5)\u00a0inhibits bone resorption by enhancing apoptosis of monocytes. Unloading exposure\u2010induced cell survival is mediated by X\u2010linked inhibitor of apoptosis protein (XIAP)\/direct IAP binding protein with low pI (Diablo) axis. Upon mechanical unloading XIAP is upregulated, then interacts with Diablo in mitochondrial and promotes the K63\u2010linkage ubiquitylation of Diablo at the K212 site. This sequesters Diablo within the mitochondrial and inhibits its release into the cytosol, ultimately inhibiting cell apoptosis of osteoclasts and the precursors. Clinically, the serum Gln levels are positively correlated with cross linked C\u2010telopeptide of type I collagen (CTX) levels, indicating that serum Gln levels might serve as a potential biomarker for predicting the risk of osteoporosis. Gln\u2010deficient diet, as well as SLC1A5 inhibitor L\u2010\u03b3\u2010Glutamyl\u2010p\u2010nitroanilide (GPNA), effectively preserves bone mass in HLU mice, implicating attractive approaches for combating bone loss induced by weightlessness or disuse.<\/jats:p>","DOI":"10.1002\/advs.202500585","type":"journal-article","created":{"date-parts":[[2025,8,18]],"date-time":"2025-08-18T08:59:02Z","timestamp":1755507542000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Integrative Omics Reveals Glutamine Catabolism\u2010Driven Apoptotic Suppression in Monocytes upon Mechanical Unloading"],"prefix":"10.1002","volume":"12","author":[{"given":"Yi","family":"Ding","sequence":"first","affiliation":[{"name":"State Key Laboratory of Medical Proteomics Beijing Proteome Research Center National Center for Protein Sciences (Beijing) Beijing Institute of Lifeomics  Beijing 102206 China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fan","family":"Tong","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Medical Proteomics Beijing Proteome Research Center National Center for Protein Sciences (Beijing) Beijing Institute of Lifeomics  Beijing 102206 China"},{"name":"School of Basic Medical Sciences Anhui Medical University  Hefei Anhui 230022 China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mingqiu","family":"Liu","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Medical Proteomics Beijing Proteome Research Center National Center for Protein Sciences (Beijing) Beijing Institute of Lifeomics  Beijing 102206 China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pin","family":"Yang","sequence":"additional","affiliation":[{"name":"School of Basic Medical Sciences Anhui Medical University  Hefei Anhui 230022 China"},{"name":"Bioinformatics Center of AMMS  Beijing 100850 China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Zeng","sequence":"additional","affiliation":[{"name":"Department of Endocrinology The Second Medical Center &amp; 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