UCLA

It was hypothesized that IR triggered premature senescence in dental pulp, resulting in loss of mineralization potential and enhanced expression of senescence-associated inflammation. It was found that IR induced premature senescence and phenotypic alterations in DPSCs in terms of mineralization potential and inflammatory response. Furthermore, IR also led to DNA damage in the dental pulp cells in vivo. It was demonstrated that the application of Yel2, a promising radioprotector, mitigated IR induced premature senescence and DNA damage. These findings elucidated the molecular mechanism by which dental pulp cells responded to IR and may have potentials in advancing therapies for irradiated patients.