Bach2 regulates autophagy to modulate UVA-induced photoaging in skin fibroblasts

Senescence is a cellular process that can be initiated by certain stressors such as UVA irradiation. The mechanism which skin cells protect themselves from the UVA-induced senescence has not been fully investigated. Here, we demonstrate Bach2 modulates extent of photoaging through regulation autophagy in fibroblasts. In fact chronic exposure fibroblasts to resulted significant decrease expression, both vitro and vivo. addition, knockdown led an increased expression cell senescence-related genes, further enhanced irradiation-induced photoaging. On other hand, overexpression genes. We also lead decreased autophagy-related genes vice versa, suggesting involved Bach2-mediated Additionally, inhibition with inhibitor 3-MA suppressed proteins promoted senescence. Furthermore, knockout Atg5 or Atg7 embryonic mouse increase Immunoprecipitation assays demonstrated directly interacts Beclin-1, Atg3, Atg7, LC3 Taken together, these findings revealed critical role for suppressing via therefore potential target therapy UV-induced because its ability regulate skin.