The purinergic receptor P2rx7 mediated ATP sensing is required to prevent bone aging by directing mitochondrial fitness of MSCs

Bone aging contributes to osteoporosis and impaired bone formation, mechanisms intricately linked to alterations in mesenchymal stem cells (MSCs) that include a metabolic decline whose precise mechanisms remain elusive. In this study, P2rx7 was identified as a key regulator of mitochondrial fitness in bone marrow MSCs during the bone aging process. To validate the role of P2rx7 in bone metabolism and aging, we deleted P2rx7 by using P2rx7 knockout mice and the mice demonstrated premature and exacerbated bone aging. What we want to explore is how P2rx7 knockout affects the genome changes of bone cells. To investigate how P2rx7 knockout influenced the bone, we constructed P2rx7 knockout mice. Femurs of three different Wildtype (WT) mice or P2rx7 knockout mice aged 6-8 weeks were collected the bone marrow were flushed out and used for RNA-seq.