UVA irradiation may initiate cellular process like Senescence. It is still unclear how the skin cells protect themselves from the UVA-induced.

Wang M. et al demonstrated that Bach2 modulates the extent of UVA-induced photoaging through regulation of autophagy in skin fibroblasts. 

They found that when skin fibroblasts are chronically exposed to UVA, the Bach2 expression decreases, both in vitro and in vivo. Additionally, knockdown of Bach2 in skin fibroblasts causes increased expression of cell senescence-related genes, further enhancing the UVA irradiation-induced photoaging. while the overexpression of Bach2 causes decreases expression of cell senescence-related genes. Thus it is true both ways.

The study also highlights that knockdown of Bach2 in skin fibroblasts causes decreased expression of autophagy-related genes and vice versa, indicating the role of autophagy in Bach2-mediated regulation of senescence in skin fibroblasts. 

They also mentioned that-

• Inhibition of autophagy with autophagy inhibitor 3-MA decreased the expression of autophagy-related proteins and encouraged cell senescence.
• Knockout of Atg5 or Atg7 in embryonic mouse fibroblasts caused remarkable elevation in the expression of cell senescence-related genes.
• Immunoprecipitation assays demonstrated direct interaction of Bach2 with Beclin-1, Atg3, Atg7, and LC3 in fibroblasts. 

Thus they supported the critical role for Bach2 in suppressing the UVA irradiation-induced cell senescence via autophagy in skin fibroblasts and advocated Bach2 to be a potential target for the therapy of UV-induced photoaging pertaining to its ability to regulate the process of autophagy in the skin.

Source: Wang M, Lei M, Chang L, Xing Y, Guo Y, Pourzand C, Bartsch JW, Chen J, Luo J, WidyaKarisma V, Nisar MF, Lei X, Zhong JL. Bach2 regulates autophagy to modulate UVA-induced photoaging in skin fibroblasts. Free Radic Biol Med. 2021 Apr 18;169:304-316. doi: 10.1016/j.freeradbiomed.2021.04.003. Epub ahead of print. PMID: 33882335.