Stratum corneum proteases and dry skin conditions

• Published in: Cell and tissue research Vol. 351; no. 2; pp. 217 - 235
• Main Authors: Rawlings, Anthony V., Voegeli, Rainer
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer-Verlag 01.02.2013; Springer; Springer Nature B.V
• Subjects: Animals; Atopic dermatitis; Biomedical and Life Sciences; Biomedicine; Care and treatment; Epidermis - cytology; Epidermis - enzymology; Human Genetics; Humans; Medical treatment; Molecular Medicine; Peptide Hydrolases - metabolism; Proteases; Proteomics; Psoriasis; Review; Skin; Skin - cytology; Skin - enzymology; Skin care products; Skin diseases; Skin Diseases - enzymology; Skin Diseases - pathology; Stratum corneum; Desquamation; Proteases; Corneotherapy; Corneocare
• ISSN: 0302-766X; 1432-0878
• DOI: 10.1007/s00441-012-1501-x

This paper reviews the role of stratum corneum (SC) proteases and their inhibitors in normal and xerotic skin conditions. The importance of the corneodesmosome for SC integrity is also discussed, and the effect of proteases on its disassembly. The relevance of each enzyme class is outlined, as well as their potential inhibitors. It is becoming much clearer, however, that the LEKTI family of inhibitors are critical for SC enzyme control. Delayed desquamation is the accumulation of corneocytes on the surface of the SC that leads ultimately to the cosmetic condition commonly termed as “dry skin”. The reductions of serine protease activity are a consistent theme in dry skin, and non-eczematous atopic dermatitis otherwise known as atopic xerosis leading to retention hyperkeratosis. Flaky skin is normally seen on the body whereas a rough skin is observed on the face. Increased protease activity occurs in most, if not all, inflammatory dermatoses, ranging from the genetic disorders, psoriasis and eczematous atopic dermatitis to sub-clinical barrier abnormalities induced by surfactants or by environmental influences as a result of premature desquamation. In some of these conditions a thinner SC is apparent, e.g., eczematous atopic skin or on photodamaged facial skin. A better understanding of the proteolytic events and of the regulatory mechanisms involved in desquamation should enable the design of new treatments for skin disorders associated with faulty desquamation. This new knowledge will be an important basis for new developments in ‘corneotherapy’ and ‘corneocare’.