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Comedogenesis refers to the process underlying the formation of comedones—clogged hair follicles or pores that result when keratin (skin debris) combines with sebum (skin oil) to block follicular openings[7][6]. This process is central to the pathophysiology of acne but is not attributable to a single molecular entity. The term "comedogenic" also refers to substances or conditions (e.g., certain skincare ingredients or hormonal changes) that promote this process by disrupting normal keratinization or increasing sebum production[9][8][10]. The main events in comedogenesis are: (1) increased sebum production, (2) abnormal keratinocyte proliferation/keratinization, and (3) blockage of the pilosebaceous duct[1][3][5][6]. Androgens (hormones) stimulate sebum production and can enhance the process, and cytokines such as IL-1α and IL-1β are implicated as mediators that further promote keratinocyte proliferation and comedone formation[1]. While comedogenesis underlies acne pathogenesis, it is a complex multi-cellular process—not a discrete molecular target for drug intervention[1][2][3][4][5][6][7][9][10].
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