SYSTEMATIC REVIEW article
Front. Immunol.
Sec. Autoimmune and Autoinflammatory Disorders : Autoimmune Disorders
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1669382
This article is part of the Research TopicMolecular Characterisation of Autoimmune DiseasesView all 11 articles
The Role of MicroRNAs in Primary Sjögren's Disease: Deciphering Regulatory Networks and Assessing Current Therapeutic Perspectives
Provisionally accepted- 1The Rheumatology Department of the First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou City, China
- 2Henan University of Chinese Medicine Henan Provincial Hospital of TCM, Zhengzhou, China
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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.
Keywords: microRNA, Primary Sjögren's Disease, regulatory networks, Therapeutic perspectives, Macrophage polarization, Apoptosis, Th17/Treg balance
Received: 19 Jul 2025; Accepted: 29 Sep 2025.
Copyright: © 2025 Wang, Li, LIU, Du and Li. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Songwei Li, ryanzzdx@yeah.net
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