Skin keratinocytes proliferation pathway

The "Skin keratinocytes proliferation pathway" is not a single molecule, receptor, or enzyme, but encompasses a network of signaling and metabolic processes controlling the renewal of keratinocytes in the epidermis. Key regulators include growth factors, cytokines, and signaling pathways (e.g., Notch, Wnt/β-catenin, TGF-β, JAK/STAT) that integrate signals from the microenvironment, immune cells, and metabolic cues (like glycolysis) to balance proliferation and differentiation of keratinocytes[1][3][4][5][7]. Disruption of these pathways underlies skin pathologies such as psoriasis (characterized by hyperproliferation), wound healing disorders, and some cancers. Since this is an umbrella term for multiple interacting processes, it is not a valid therapeutic 'target' in the conventional pharmacological sense, nor does it have a canonical abbreviation, molecular classification, or direct drug interactors. Note: If a specific molecule, receptor, or gene in the keratinocyte proliferation pathway is of interest (e.g., "Notch1," "EGFR," "JAK2," "p63," "FBP1"), please specify, as those are considered valid drug targets.

Other names

Keratinocyte proliferationKeratinocyte cell cycle pathwaysEpidermal proliferation signaling

Not applicable for a pathway as a molecular target; related drugs act via modulating growth factors, cytokines (e.g., IL-6, TNF-α, IL-17), and interfering with signaling pathways (e.g., JAK-STAT, Notch, Wnt/β-catenin)[1][4][7].