Mecanismos epigenéticos asociados a la patogenia de la enfermedad de lupus eritematoso sistémico: una revisión de tema

Introduction: Systemic Lupus Erythematosus (SLE) is a prevalent autoimmune disease characterized by a dysregulated immune response against multiple autoantigens. While the etiology of SLE is complex and multifac-torial, epigenetics has emerged as a relevant explanation for its underlying mechanisms. Objective: To analyze and describe the epigenetic mechanisms associated with the pathophysiology of SLE. Methods: A literature review was conducted to identify associations between epigenetic mechanisms and the pathophysiology of SLE, focusing on the recognition of key markers. Results: Downregulation of DNA methylation allows for the expression of genes that increase susceptibility to autoantigen presentation and autoantibody generation. Additionally, modifications of histones H3K4me1 and H3Kme2 facilitate chromatin decondensation, increasing the transcription of genes that promote cell growth and proliferation, such as CDKN2A, PTPN22, and LRP1B, while condensing chromatin of regulatory genes like RUNX3. Furthermore, miRNAs such as miR-146a, miR21, and miR148a have been associated with abnormal inflammatory cascades, alterations in the interferon pathway, and DNA methylation. Conclusions: Epigenetic mechanisms appear to be pivotal in the initiation of autoimmune pathologies and the environmental susceptibility of these patients.