MicroRNAs in systemic lupus erythematosus: Molecular networks, pathway dysregulation, and therapeutic targeting strategies
TL;DR
The role of miRNAs in SLE pathogenesis, their potential as biomarkers, and their emerging relevance as therapeutic targets are highlighted, while also addressing current limitations and challenges in clinical translation are addressed.
Abstract
Systemic lupus erythematosus (SLE) is a complex autoimmune disorder characterized by immune dysregulation, chronic inflammation, and multi-organ involvement. Its pathogenesis is multifactorial, involving genetic, epigenetic, and environmental factors that collectively contribute to the loss of immune tolerance. In recent years, considerable attention has focused on epigenetic mechanisms, particularly microRNAs (miRNAs), which function as post-transcriptional regulators of gene expression and play pivotal roles in immune cell differentiation and function. Emerging evidence suggests that dysregulated expressions of specific miRNAs, such as miR-146a and miR-155, may contribute to aberrant immune responses, including altered T- and B-cell activity and cytokine production in SLE. These alterations have been associated with disease activity and immunopathological processes. In addition, circulating miRNAs have been investigated as potential non-invasive biomarkers for diagnosis and disease monitoring. Advances in high-throughput technologies have facilitated the identification of miRNA expression profiles associated with SLE; however, variability between studies and limited clinical validation remain challenges. While miRNA-based therapeutic strategies are being explored, their clinical application is still under investigation. This review highlights the role of miRNAs in SLE pathogenesis, their potential as biomarkers, and their emerging relevance as therapeutic targets, while also addressing current limitations and challenges in clinical translation.