MINI REVIEW article
Front. Med.
Sec. Dermatology
Volume 12 - 2025 | doi: 10.3389/fmed.2025.1585525
Barium and Psoriasis: A Mini-Review and Hypothesis Linking Environmental Exposures to Ion Channel Modulation
Provisionally accepted- 1National Institutes of Health (NIH), Bethesda, United States
- 2University of Florida, Gainesville, Florida, United States
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Psoriasis is a complex autoimmune skin disorder with rising prevalence and significant comorbidities. Although its etiology remains multifactorial, recent epidemiologic and mechanistic studies -including the NHANES-based analysis by Chen et al. -suggest that environmental exposures, particularly to heavy metals may contribute to its pathogenesis. To further understand this association, we reviewed current literature on the pathogenesis of psoriasis and relevant ion channels, as well as the interactions of both with the heavy metal barium. Both epidemiologic and laboratory data highlight a potential link between environmental heavy metal exposure and autoimmune dysregulation in psoriasis. This review offers a novel hypothesis that mechanistically links environmental exposures to psoriasis through ion channel modulation. Further research is warranted to elucidate the precise mechanisms by which barium can influence K⁺ channel function and inflammasome activation, potentially offering new approaches for therapeutic interventions in psoriasis and other autoimmune disorders.
Keywords: Psoriasis, Kv1.3, KCa3.1, Barium, Inflammation
Received: 28 Feb 2025; Accepted: 03 Jun 2025.
Copyright: © 2025 Myles, Zeldin, Jordan, Thota, Vuong and Jojo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Ian A Myles, National Institutes of Health (NIH), Bethesda, United States
Jordan Zeldin, National Institutes of Health (NIH), Bethesda, United States
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