Filaggrin: a key to understanding and treating atopic dermatitis

Atopic dermatitis is a chronic inflammatory genetically determined skin disease characterized by high prevalence and a significant negative impact on patients’ quality of life. Impairment of the skin barrier in atopic dermatitis is closely associated with filaggrin deficiency—a key structural protein of the epidermis. Loss-of-function mutations in the FLG gene are a major genetic risk factor for atopic dermatitis, significantly worsening its course and prognosis. Currently, active research is underway to develop effective methods for restoring filaggrin deficiency, which represents a promising approach in the therapy of atopic dermatitis. This article provides a systematic scientific data analysis in the PubMed, Google Scholar, and ClinicalTrials.gov databases to identify modern approaches to restoring the skin barrier in atopic dermatitis by targeting filaggrin and its metabolism. The following promising strategies for targeting filaggrin have been identified: direct replacement therapy with recombinant forms of filaggrin, the use of metabolites (L-histidine, cis-urocanic acid), plant extracts, and mechanical stimulation methods. These approaches demonstrate the potential to improve skin barrier function and reduce inflammation; however, further studies are needed to confirm their clinical efficacy and clarify mechanisms of action. Modern strategies for correcting filaggrin deficiency hold significant therapeutic potential for atopic dermatitis but require further research, including at the molecular and clinical levels, to enable their integration into clinical practice.