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Skin desquamation is the physiological process involving the shedding of the outermost layer of the epidermis, the stratum corneum, to maintain skin homeostasis and barrier integrity (StatPearls, NBK545181). This process is regulated by a complex interplay of proteolytic enzymes, specifically kallikrein-related peptidases (such as KLK5, KLK7, and KLK14), which degrade the corneodesmosomes that anchor corneocytes together (PubMed, PMID: 16528362). Dysregulation of desquamation is central to the pathogenesis of several dermatological conditions, including ichthyosis, where impaired shedding leads to scale accumulation, and psoriasis, characterized by hyperproliferation and abnormal maturation (NIH, StatPearls). While desquamation itself is a biological phenomenon rather than a single molecular target, its underlying pathways are modulated by therapeutic agents such as keratolytics (e.g., salicylic acid) and retinoids (e.g., tretinoin) to restore normal epidermal turnover (PubMed, PMID: 22409454). Therapeutic strategies often focus on either enhancing desquamation in hyperkeratotic states or protecting the barrier in inflammatory conditions where shedding is premature. Monitoring biomarkers like transepidermal water loss (TEWL) and protease activity is essential for assessing the efficacy of treatments targeting these pathways (PubMed, PMID: 15675888).
Keratolytic agents and retinoids modulate corneocyte adhesion and epidermal differentiation to normalize the shedding process (PubMed, PMID: 22409454).
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