特应性皮炎（AD）前沿文献精读特辑（Exp Dermatol / J Dermatol Sci / J Eur Acad Dermatol Venereol）

Autophagy is increasingly recognised as a regulator of epithelial stress adaptation in the skin, but its role in inflammatory dermatoses remains difficult to interpret because autophagy intersects with barrier biology, keratinocyte differentiation, immune signalling, intracellular trafficking and lysosomal degradation. Keratinocytes are immune-competent epithelial cells that integrate cytokine exposure, oxidative stress, microbial sensing and tissue injury into inflammatory output. In this review, we synthesize evidence on keratinocyte autophagy as a disease-dependent regulator of epidermal homeostasis and cutaneous inflammation. We summarize core autophagy machinery, selective autophagy programs relevant to epidermal differentiation and the interpretive value of autophagic flux and lysosomal competence. We then discuss how autophagy influences keratinocyte differentiation, organelle clearance, lipid handling, barrier support, inflammatory restraint and stress adaptation. Disease-specific evidence is reviewed in psoriasis, AP1S3-associated pustular autoinflammation, atopic dermatitis and vitiligo. Across these settings, keratinocyte autophagy cannot be classified as uniformly protective or pathogenic; its effects depend on inflammatory context, trafficking state, cell-type-specific outputs and the ability of lysosomes to complete degradation. We also consider lessons from other barrier epithelia, therapeutic implications and common methodological limitations. A keratinocyte-centered, flux-aware interpretation provides a framework for organizing disease-specific autophagy biology and for designing more rigorous mechanistic studies in inflammatory dermatoses.

Autophagy, a highly conserved cellular degradation process, is essential for maintaining cellular homeostasis and responding to stress. Recent studies have highlighted the importance of autophagy in regulating epidermal functions, including keratinocyte differentiation and proliferation, epidermal lipid synthesis, inflammation, and antioxidation. In the epidermis, autophagy facilitates the removal of damaged organelles and protein aggregates, ensuring proper keratinocyte maturation and stratum corneum formation. Dysregulation of autophagy has been linked to various dermatological conditions, such as psoriasis, atopic dermatitis, and skin aging. Furthermore, autophagy modulates the inflammatory response in the skin by regulating cytokine production and immune cell activity. This review summarizes evidence supporting the role of autophagy in epidermal function and emphasizes its potential as a therapeutic target. Additionally, approaches to enhance autophagy are discussed.