<p>Ferroptosis represents an iron-dependent cell death pathway driven by lipid peroxide accumulation. Recent research has established that ferroptosis is closely linked to the pathogenesis and progression of various autoimmune and inflammatory skin diseases. This article systematically reviews the biological basis of ferroptosis and its specific regulatory characteristics in the skin, focusing on three core mechanisms: iron metabolism, lipid metabolism, and redox homeostasis. It emphasizes the hierarchical, dynamic, and complex nature of the skin, as a barrier organ exposed to the external environment, in maintaining ferroptosis homeostasis. This article focuses on representative diseases such as psoriasis, systemic lupus erythematosus, vitiligo, systemic sclerosis, photodermatoses, and atopic dermatitis. It summarizes the mechanisms by which ferroptosis is involved in skin cell injury, immune activation, inflammation maintenance, and autoantigen exposure. Finally, considering the current research limitations and gaps, the article proposes the potential of ferroptosis as a therapeutic target for autoimmune and inflammatory skin diseases.</p>