We've Misunderstood How Sunburns Actually Work

RNA damage, rather than DNA damage, is the key source of sun exposure's immediate inflammatory effects.
RNA damage, rather than DNA damage, is the key source of sun exposure's immediate inflammatory effects.
SHOTPRIME STUDIO at Adobe Stock

A fascinating study from the journal Molecular Cell argues that, while DNA damage resulting from solar UVB exposure remains a concern long-term, it is in fact RNA molecule damage, via the ribotoxic stress response, that induces immediate sunburn symptoms.

The key culprit? ZAK-alpha, a protein that induces the skin's protective response.

Per the authors, "skin cells rely on a cytoplasmic and ribosomal stress signal rather than a nuclear and DNA-templated signal for rapid inflammatory responses to UV exposure."

The result of the ribotoxic stress response is "dermal inflammation, keratinocyte cell death and epidermal thickening," per the report.

DNA damage is a key target for brands seeking to prevent or diminish photoaging; this new research could shed new light on targets for preventing immediate solar UVB damage.

Read the full study here.


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