Rosacea is a chronic inflammatory disease of the facial skin characterized by high prevalence among people of active age. Its development is a multifactorial process caused by complex interactions of genetic predisposition, immune mechanisms, vascular hyperreactivity and numerous lifestyle and environmental factors. In rosacea pathogenesis, a special role is given to the activation of mechanisms of immune inflammation, which is carried out with the involvement of toll-like receptors 2 (TLR2) and cathelicidin LL-37, promoting the production of active forms of oxygen and increase of the expression of anti-inflammatory cytokines and matrix metalloproteinases. Disruption of the epidermal barrier function, formed by transepidermal water loss, increased skin pH and exposure to ultraviolet radiation, is an important component of the pathological process in rosacea. Published data show the association of rosacea development with vascular homeostasis abnormality and vasodilation, mediated by the action of transient receptor potential channels, as well as the density of skin colonization by Demodex mites, promoting the activation of TLR2 and production of inflammation mediators. Currently, topical and systemic drugs are the basis of rosacea therapy. Agents that provide antiparasitic (ivermectin) and antimicrobial (metronidazole, benzoyl peroxide) action, KLK5 inhibitors (azelaic acid) and α₂-adrenergic receptor agonists (brimonidine, oxymetazoline) are used for topical therapy. Rosacea systemic therapy regimens may include antibacterial drugs (doxycycline, minocycline, azithromycin), retinoids (isotretinoin) as well as β-adrenergic receptor agonists (propranolol, carvedilol). In resistant and severe forms of pathological process, it is advisable to prescribe combination therapy schemes including topical agents, systemic drugs and (or) methods based on the use of preformed physical factors. It is becoming increasingly important to search for new treatment methods focused on the various components of disease pathogenesis.