
Frontiers in Genetics, Journal Year: 2025, Volume and Issue: 16
Published: March 27, 2025
Idiopathic Pulmonary Fibrosis (IPF) is a progressive interstitial lung disease characterized by unknown etiology and limited therapeutic options. Recent studies implicate exosomal non-coding RNAs (ncRNAs) as crucial regulators in IPF. These ncRNAs, including long (lncRNAs), microRNAs (miRNAs), circular (circRNAs), are involved cellular processes through various mechanisms of selective packaging, intercellular communication, signaling pathway integration. LncRNAs such LINC00470 PVT1 exhibit pro-fibrotic effects, while others like lnc-DC THRIL show inhibitory roles; some, UCA1 MALAT1, demonstrate bidirectional regulation. In miRNAs, agents (e.g., miR-486, miR-223) contrast with miRNAs miR-34a, miR-126), miR-21 miR-155 display dual functions. Similarly, circRNAs circ_0000479 circ_0026344 promote fibrosis, whereas circ_0000072 circ_0000410 act inhibitors, certain circ_002178 circ_0001246) exhibiting complex regulatory effects. Exosomal ncRNAs modulate key pathways, TGF-β Wnt/β-catenin, influencing IPF progression. Despite their potential, challenges remain exosome isolation, functional characterization clinical translation. Addressing these barriers innovative research strategies essential to leverage the management treatment This review comprehensively examines roles IPF, elucidates interactions, discusses future perspectives enhance understanding for this disease.
Language: Английский