The study identifies DEL-1 as an endogenous senolytic factor that selectively eliminates senescent osteoprogenitor cells and protects against age-associated bone loss. DEL-1 reduced senescence markers, improved osteogenic differentiation, and attenuated inflammatory SASP signaling. In vivo administration preserved bone mass and reduced osteoclastogenic activity in aged and osteoporosis models.
DEL-1 reduced senescent cell burden, suppressed SASP-associated inflammation, preserved bone density, and improved osteogenic activity. Loss of DEL-1 accelerated bone degeneration and inflammatory remodeling.
Del1 Knockout mouse and DEL-1-treated aging bone loss models
Senescence, osteoporosis, bone aging, osteoimmunology, senolytic therapy, skeletal degeneration
Del1 Knockout model, aging-associated bone loss analysis, osteogenic differentiation assays, senescence marker quantification, SASP profiling, bone micro-CT analysis, osteoclast activity measurements
From model design to experimental results
Featured in 600+ scientific articles
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Models with certified health status from professional breeders in US and Europe
