Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0152030 (skin irritation)
 2,146 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute perturbations are followed by barrier repair and enhanced lipid synthesis, as well as cellular fatty acid trafficking, yet irritation of the skin may be induced by repeat disturbance of barrier function. Recently, new insights in cellular fatty acid transport and metabolism have evolved with respect to skin irritation and barrier disturbances: (1) Employing sodium dodecyl sulfate, skin irritation is accompanied by the induction of an epidermal (E) cytosolic fatty acid binding protein (FABP) associated with enhanced barrier repair. Whether E-FABP contributes to the water barrier function in normal skin remains to be elucidated; (2) Cutaneous inflammation, as it occurs in irritant contact dermatitis, can be reduced by peroxisome proliferating activated receptor (PPAR) agonists, such as linoleic acid, with clinical effects comparable to that of glucocorticoids; (3) PPARalpha agonists accelerate barrier recovery and enhance lamellar body synthesis, neutral lipid synthesis, in particular that of ceramides and cholesterol; (4) PPARalpha agonists increase the minimal erythema dose in UVB-irradiated human skin. This review provides a brief overview of the current understanding of mammalian fatty acid (FA) metabolism with respect to epidermal barrier abrogation and repair, including new insights into cellular FA transport and metabolism.
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PMID:Implementation of fatty acid carriers to skin irritation and the epidermal barrier. 1249 17

The exact role of epidermal fatty acid binding protein (E-FABP) in skin is unknown. A restoration of the barrier function may be associated with an upregulation of E-FABP. Moreover, E-FABP is upregulated in a variety of cells in response to oxidative stress. A recent observation that dithranol induced irritation is not associated with skin barrier impairment prompted us to investigate the expression of E-FABP in this skin condition to elucidate the unknown function of this protein in skin. This study shows lack of E-FABP upregulation after a single application of dithranol on uninvolved skin of patients with psoriasis. The expression of E-FABP in dithranol irritation correlates with the unimpaired skin barrier function as assessed by measurements of TEWL. Furthermore, we did not find evidence for the recently introduced hypothesis that E-FABP functions as an antioxidant protein in the skin irritation induced by dithranol as oxidative stressor.
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PMID:Lack of upregulation of epidermal fatty acid binding protein in dithranol induced irritation. 1280 84