ArticleMolecular genetics and genomics : MGG2026
USP22 alleviates oxidative stress-induced BMSCs senescence by stabilizing SPI1 protein.
Article in Molecular genetics and genomics : MGG, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundTherapeutic efficacy of bone marrow mesenchymal stem cell (BMSC) transplantation is often compromised by cellular senescence and diminished osteogenic potential induced by oxidative stress. Nevertheless, the underlying molecular mechanisms remain poorly understood. This study explores the role of ubiquitin-specific peptidase 22 (USP22) in regulating oxidative stress-induced BMSCs senescence.
methodsBMSCs were exposed to H
resultsSPI1 expression declined in H
conclusionUSP22 mitigated oxidative stress-induced BMSCs senescence and preserved osteogenic capacity by promoting NAMPT transcription through deubiquitinating and stabilizing SPI1 protein.
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