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Keratin and intercellular desmosomes constitute the primary structural framework of the epidermis, providing the mechanical strength and cohesive properties necessary for the skin's barrier function. Keratins are a diverse group of intermediate filament proteins that form the internal cytoskeleton of keratinocytes, while desmosomes are specialized cell-to-cell junctions that anchor these filaments to the plasma membrane, linking adjacent cells together (StatPearls: Histology, Desmosomes [1]). In pathological states such as hyperkeratosis, there is an abnormal accumulation of keratin and a failure of desmosomal degradation, resulting in a thickened and dysfunctional stratum corneum (NCBI: Hyperkeratosis [2]). Therapeutic strategies targeting these structures primarily utilize keratolytic agents, such as salicylic acid and urea, which act by disrupting the adhesive bonds of desmosomes and denaturing keratin proteins to facilitate desquamation (PubChem: Salicylic Acid [3]). By reducing the cohesion between corneocytes, these treatments help restore normal epidermal thickness and improve the penetration of other topical medications. While effective for conditions like psoriasis and ichthyosis, over-treatment can lead to significant skin irritation and a compromised barrier, highlighting the need for precise modulation of these structural components (PubMed: Keratolytic mechanisms [4]).
Keratolytic agents promote the dissolution of the intercellular matrix (desmosomes) and the softening of keratin, leading to increased hydration and the shedding of the stratum corneum.
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