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The **skin barrier** refers primarily to the outermost layer of the epidermis—the stratum corneum—which acts as a critical physical and biochemical shield between the body and its environment. This structure is composed of flattened dead cells called corneocytes embedded in a matrix of specialized lipids including ceramides, cholesterol, and free fatty acids[2][3][4][6]. The "bricks-and-mortar" model describes how protein-rich corneocytes ("bricks") are surrounded by lipid layers ("mortar"), creating a highly ordered lamellar structure that prevents excessive water loss from within while blocking entry of pathogens, allergens, irritants, and toxins from outside[3][5][7]. The skin's protective function also relies on additional elements such as the acid mantle—a mildly acidic hydrolipid film that supports beneficial microbial flora—and immune components within deeper layers[3]. Disruption or deficiency in any component—such as altered lipid composition or mutations in structural proteins—can lead to increased permeability ("leaky" skin), resulting in conditions like atopic dermatitis or increased susceptibility to infection[1][4][6]. **Note:** "Skin barrier protection" is not a single molecule or receptor but rather an emergent property arising from complex interactions among multiple molecular structures (lipids, proteins) within the stratum corneum. It does not correspond to a canonical drug target such as an enzyme or receptor; therefore it should not be classified as one for structured data purposes. If you are seeking information about specific molecular targets involved in regulating or maintaining the skin barrier—such as filaggrin or histone deacetylase 3 (HDAC3)—those should be specified individually for accurate mapping[1].
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