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A deeper understanding of acne pathogenesis enables a more personalized approach to treatment, encompassing not only pharmacotherapy but also dietary interventions and skincare routines. Objective. To summarize research findings on the molecular and biological mechanisms of acne pathogenesis and to evaluate the effect of isotretinoin (an active vitamin A derivative) on its development and course, given that this specific substance is the most effective treatment for severe forms of the disease. The study examines the key molecular and biological pathways in the pathogenesis of acne, where elevated levels of insulin-like growth factor 1 or sex hormone imbalances — acting through intracellular signaling pathways driven by protein-protein interactions in sebocytes and keratinocytes — promote follicular hyperkeratosis, hyperseborrhea, and cutaneous inflammation. These pathological processes can expand the population of virulent Cutibacterium acnes phylotypes, thereby exacerbating the disease severity by promoting inflammation and follicular hyperkeratosis. The primary pathogenetic mechanism may vary among patients. Isotretinoin counteracts the key mechanisms of acne pathogenesis through its effects on the cellular genome. It can be administered either topically or systemically depending on the severity of the disease.
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Petrova et al. (2026) studied this question.
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