AI Article Synopsis
- Seborrheic keratosis is a benign skin tumor common in older adults and is often pigmented, with evidence linking high uric acid levels to related skin conditions like acanthosis nigricans.
- Research confirms that uric acid, produced by keratinocytes, contributes to melanocyte activity by increasing key proteins (MITF and tyrosinase), promoting hyperpigmentation.
- The process involves uric acid transport out of keratinocytes and uptake by melanocytes, activating pathways that enhance melanin production, indicating a connection between seborrheic keratosis and skin pigmentation changes due to aging and UV damage.
Article Abstract
Seborrheic keratosis, which is a benign tumor composed of epidermal keratinocytes, develops common in the elderly. Uric acid generated by upregulated guanine deaminase () has been identified to cause UV-induced keratinocyte senescence in seborrheic keratosis. Seborrheic keratosis is also frequently pigmented. Growing evidences indicate that hyperuricemia is a risk factor of acanthosis nigricans, an acquired skin hyperpigmentation. The objective of this study was to investigate role of and its metabolic end product, uric acid, in hyperpigmentation of patients with seborrheic keratosis using their lesional and non-lesional skin specimen sets and cultured primary human epidermal keratinocytes with or without overexpression or uric acid treatment. -overexpressing keratinocytes or their conditioned media containing uric acid increased expression levels of MITF and tyrosinase in melanocytes. Uric acid released from keratinocytes was facilitated by ABCG2 transporter with the help of PDZK1 interaction. Released uric acid was taken by URAT1 transporter in melanocytes, stimulating melanogenesis through p38 MAPK activation. Overall, upregulation in seborrheic keratosis plays a role in melanogenesis via its metabolic end product uric acid, suggesting that seborrheic keratosis as an example of hyperpigmentation associated with photoaging.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8625227 | PMC |
| http://dx.doi.org/10.3390/ijms222212501 | DOI Listing |
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