Functional roles of microRNAs in pancreatic islet autoimmunity: what do we know and where do we target?

INTRODUCTION

Type 1 diabetes (T1D) results from a destructive dialog between stressed pancreatic beta-cells and immune system. While current disease-modifying approaches targeting these processes are being developed and tested, microRNAs have emerged as a molecular interface connecting both sides of islet autoimmunity.

AREAS COVERED: Specific miRNAs orchestrate beta-cell stress adaptation, immune activation, and intercellular communication, thus shaping disease trajectory and progression across stages. Recent discoveries identified distinct miRNA networks as ER-stress modulators and/or immune amplifiers and key regulators of beta-cell fate and circulating signals of ongoing inflammation.

EXPERT OPINION: The clinical translation of these insights remains hindered by limited access to human tissues, inconsistent candidate validation, and lack of delivery systems capable of targeting pancreatic beta-cells. Bridging mechanistic understanding with advanced delivery systems may transform miRNAs both as biomarkers and active therapeutic agents, opening a path toward precision interventions in T1D.