biostudies-literatureXiao HYayi Xia1801https://www.ebi.ac.uk/biostudies/studies/S-EPMC12731071biostudies-literatureUnknown14(12)<h4>Background</h4>Osteoblast senescence constitutes one of the major mechanisms in bone degeneration and is under tight regulation by metabolism and oxidative stress. While hypoxia has recently emerged as an important microenvironmental factor influencing the function of bone cells, its role in osteoblast senescence and metabolic regulation has yet to be defined.<h4>Methods</h4>The present work entails hypoxia-modulated osteoblast senescence at one level, transcriptomic and metabolomic sequencing, and two levels, in vitro MC3T3-E1 and in vivo AAV-shAtp6v1a mouse models. In transcriptome profiling, hypoxia-responsive genes were identified, whereas non-targeted metabolomics was used to uncover metabolic alterations induced by ATP6V1A knockdown. Oxidative stress and mitochondrial function weBiologyMechanistic Study of Hypoxia-Mediated Regulation of Osteoblast Senescence via ATP6V1A-Dependent Modulation of Metabolic Remodeling.PMC12731071This work was supported by The National Natural Science Foundation of China (81960403, 82060405, and 82360436); the Natural Science Foundation of Gansu Province (22JR5RA943, 22JR5RA956, and 23JRRA1500); the Lanzhou Science and Technology Plan Program (202Liu XXia YGeng BXiao HChen YChen CChen RYang CYang FfalseMechanistic Study of Hypoxia-Mediated Regulation of Osteoblast Senescence via ATP6V1A-Dependent Modulation of Metabolic Remodeling.<h4>Background</h4>Osteoblast senescence constitutes one of the major mechanisms in bone degeneration and is under tight regulation by metabolism and oxidative stress. While hypoxia has recently emerged as an important microenvironmental factor influencing the function of bone cells, its role in osteoblast senescence and metabolic regulation has yet to be defined.<h4>Methods</h4>The present work entails hypoxia-modulated osteoblast senescence at one level, transcriptomic and metabolomic sequencing, and two levels, in vitro MC3T3-E1 and in vivo AAV-shAtp6v1a mouse models. In transcriptome profiling, hypoxia-responsive genes were identified, whereas non-targeted metabolomics was used to uncover metabolic alterations induced by ATP6V1A knockdown. Oxidative stress and mitochondrial function we2025-01-01T00:00:00Z2025 Dec2026-05-28T03:17:51.432Z2026-05-28T03:08:24.565ZS-EPMC127310714146357410.3390/biology14121801