# The role of microRNAs in primary Sjögren’s disease: deciphering regulatory networks and assessing current therapeutic perspectives

## TL;DR

This paper explores how microRNAs influence the development and treatment of primary Sjögren’s disease by regulating immune and glandular functions.

## Contribution

The study identifies specific microRNAs and their regulatory roles in key signaling pathways, offering new therapeutic insights for Sjögren’s disease.

## Key findings

- Dysregulated miRNAs like miR-216a-3p, miR-31-5p, and miR-155-5p influence SjD progression through multiple mechanisms.
- These miRNAs modulate pathways such as NF-κB, JAK/STAT, and PI3K/AKT to improve immune and glandular functions.
- The findings suggest miRNAs could serve as promising therapeutic targets for SjD treatment.

## Abstract

Primary Sjögren’s disease (SjD) is a chronic systemic autoimmune disorder whose pathogenesis remains incompletely understood. Current clinical interventions demonstrate limited efficacy, yielding suboptimal therapeutic outcomes. microRNAs (miRNAs)–critical regulators of transcriptional networks–participate in SjD pathogenesis through multifaceted mechanisms. Dysregulated miRNA expression during SjD progression directly influences disease prognosis, establishing miRNAs as promising therapeutic targets. Evidence implicates macrophage polarization, apoptosis dysregulation, Th17/Treg imbalance, T/B lymphocyte dysfunction, glandular impairment, and aberrant type I interferon responses in SjD development. Notably, miR-216a-3p, miR-31-5p, and miR-155-5p modulate key signaling pathways (NF-κB, JAK/STAT, PI3K/AKT) to optimize macrophage polarization, suppress apoptosis, restore Th17/Treg equilibrium, regulate T/B lymphocyte activity, enhance glandular function, normalize type I interferon responses,thereby exerting potent anti-SjD effects. This review synthesizes recent literature to elucidate SjD pathogenesis and miRNA-mediated therapeutic mechanisms, providing a theoretical foundation for novel SjD management strategies.