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Corneodesmosomes are specialized intercellular junctions that provide the primary cohesive force between corneocytes in the stratum corneum, the outermost layer of the skin (Ishida-Yamamoto & Igawa, 2015). These structures are modified desmosomes containing unique proteins such as corneodesmosin (CDSN), alongside desmoglein 1 and desmocollin 1 (Jonca et al., 2011). The integrity of these junctions is vital for the skin's protective barrier, while their programmed degradation by serine proteases, specifically kallikrein-related peptidases (KLKs), allows for the process of desquamation (Caubet et al., 2004). Defects in corneodesmosome components or their regulatory enzymes lead to severe skin barrier diseases, including Netherton syndrome and various forms of ichthyosis (Hovnanian, 2013). In dermatology, these junctions are targeted by keratolytic agents like salicylic acid and urea, which facilitate the shedding of dead skin cells in hyperkeratotic disorders (Rawlings & Harding, 2004).
Keratolytic agents and retinoids promote the degradation of corneodesmosomal proteins or modulate the expression of proteases like kallikreins, thereby facilitating the shedding of corneocytes (desquamation) (Rawlings & Harding, 2004).
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