Fig. 1

DDR occurs after DNA damage, leading to cellular senescence. Senescent cells have several features: upregulation of the BCL-2 anti-apoptotic protein family (induces resistance to apoptosis, cells undergo oxidative damage (elevated ROS can be detected), metabolic changes (including the presence of SA-β-gal aggregates, SAHF and SASP), cell cycle arrest (p21 and p16 upregulation). Osteoblasts senesce in response to stress stimuli, and these cells likely cause an inflammatory microenvironment in bone by secreting SASP effects that disrupt bone formation and enhance osteoblast function. SASP can promote aggregation of BMSCs, which can differentiate into pre-osteoblasts and osteoblasts. HSCs can differentiate into osteoclasts BMSCs, bone-marrow-derived mesenchymal stem cells. DDR, DNA damage response. RANK, receptor activator of nuclear factor Kappa-B. RANKL, RANK ligand. ROS, reactive oxygen species. SAHF, senescence-associated heterochromatin foci. SASP senescence-associated secretory phenotype, SA-β-gal senescence-associated β-galactosidase. HSC haematopoietic stem cell