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The human stratum corneum corneodesmosomal and intercellular junction components comprise a specialized group of proteins and lipids essential for the structural integrity and barrier function of the skin's outermost layer (Ishida-Yamamoto & Igawa, 2015). The primary structural elements are corneodesmosomes, which are modified desmosomes containing proteins such as corneodesmosin (CDSN), desmoglein 1 (DSG1), and desmocollin 1 (DSC1) (Simon et al., 2001). These junctions provide strong adhesion between corneocytes, while the surrounding intercellular lipid lamellae ensure a water-impermeable barrier. The controlled degradation of these components, mediated by serine proteases like kallikrein-related peptidases 5 and 7 (KLK5, KLK7), is necessary for desquamation, the natural shedding of dead skin cells (Caubet et al., 2004). Defects in these junctional components or their regulatory enzymes lead to various skin disorders; for instance, mutations in the SPINK5 gene (which inhibits KLKs) cause Netherton syndrome, characterized by premature junctional breakdown and severe barrier loss (Hovnanian, 2013). Therapeutic targeting of these components typically involves keratolytics like salicylic acid or urea, which weaken the intercellular adhesion to treat hyperkeratotic conditions, or barrier-repair formulations designed to restore junctional stability in inflammatory dermatoses (Rawlings & Harding, 2004). Overall, these junctions are dynamic structures that balance mechanical stability with the physiological requirement for cell shedding.
Keratolysis and proteolysis of junctional proteins to facilitate desquamation and reduce stratum corneum thickness (Rawlings & Harding, 2004).
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