Sunburn, a common skin injury caused by overexposure to UV rays, is often linked to DNA damage and cell death. However, recent research challenges this traditional understanding by suggesting that RNA plays a more significant role in sunburn than previously believed.
DNA damage is typically associated with sunburn, leading to inflammation and cell death. But new findings indicate that RNA damage might be the primary offender. Assistant Professor Anna Constance Vind from the University of Copenhagen explains that while DNA damage is recognized, RNA damage triggers an immediate and efficient cellular response.
RNA, a temporary molecule crucial for protein synthesis, becomes particularly stressed during UV exposure. This stress activates a protective mechanism known as the “ribotoxic stress response,” monitored by the ZAK-alpha protein. When RNA damage occurs, cells respond by initiating inflammation and cell death to safeguard the skin.
The study, conducted in mice and human skin cells, revealed that RNA damage is the first sign of UV-induced skin damage. Without this response (as seen when the ZAK gene was disabled), cells showed no signs of inflammation or cell death.
This research challenges long-held beliefs about sunburn, suggesting that addressing RNA damage could lead to better prevention and treatment for inflammatory skin conditions. Dr. Franklin Zhong from NTU emphasized that understanding the cellular response to UV radiation opens new avenues for treating chronic skin diseases.
In conclusion, this groundbreaking study calls for updating our textbooks and rethinking how we perceive UV radiation’s effects on the skin. The findings underscore the critical role of RNA in sunburn and its implications for future research and treatment approaches.
Source: https://www.earth.com/news/main-cause-of-sunburn-finally-identified-is-rna-damage-not-dna