Hyaluronan synthase 3 (HAS3)-mediated hyaluronic acid synthesis in epidermal keratinocytes (HAS3-mediated HA synthesis (when specifically referring to the enzyme); if referring to the process: null)

Hyaluronic acid synthesis in epidermal keratinocytes is predominantly mediated by the enzyme hyaluronan synthase 3 (HAS3), which generates high molecular weight HA required for epidermal hydration, structural integrity, and repair[1][2]. Regulation of this process is influenced by cytokines (e.g., IFN-γ, IL-4, IL-13), growth factors (KGF, EGF), and retinoic acid, each of which can upregulate HAS3 transcription and activity. During skin inflammation, HAS3 expression and HA production are notably increased[1]. Terminal differentiation leads to increased extracellular secretion of hyaluronidase 1 (HYAL1), which degrades HA as pH falls during stratum corneum formation[1][2]. The tight regulation of HA synthesis and degradation supports keratinocyte proliferation, migration, differentiation, and wound healing. Aberrant HA metabolism contributes to diseases such as eczema, skin fibrosis, and aging[3][4]. Targeting HAS3 and regulators of epidermal HA metabolism may offer therapeutic potential in inflammatory skin conditions, dermal repair, and cosmetic dermatology[1][2][5].

Other names

Hyaluronan biosynthesis in keratinocytesKeratinocyte HA synthesisHAS3-dependent HA productionEpidermal HA metabolism

HAS3 induction: Increases HA production, stimulates proliferation and migration, enhances wound healing HAS3 inhibition: Reduces HA content, impairs barrier function, affects thickness of epidermis HA augmentation: Topical or injectable HA for hydration, anti-aging, and wound healing