Exosome-derived ncRNAs and proteins: inflammation regulatory mechanisms and biomarker potential in spinal cord injury

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Objective Exosomes, as key intercellular communication carriers, can deliver non-coding RNAs (ncRNAs) and proteins to regulate inflammatory networks, but the molecular mechanisms underlying their regulation of macrophage polarization in Spinal cord injury (SCI) remain to be systematically elucidated. This review is to interpret the molecular mechanism of exosomal ncRNA/protein regulating macrophage polarization and inflammatory network in SCI-associated neuroinflammation, and summarize its potential as a therapeutic target. Methods We screened PubMed and Embase databases from January 2010 to January 2026 to search for published studies. The search keywords used are as follows: ["exosome cargo" or "exosome"], [ncRNA"], ["spinal cord injury" or "SCI"], ["immune regulation"], ["inflammatory reaction"], ["neuroregeneration" or "nerve"]. 151 peer-reviewed studies on human/animal models were included, and articles that did not meet the requirements were excluded. Results Exosomes drive SCI pathology via multi-layered molecular networks: Pro-inflammatory exosomal miR-155-5p activates NF-κB/NLRP3 by inhibiting FoxO3a, promoting M1 macrophage polarization and TNF-α/IL-1β/IL-6 release, exacerbating neuronal pyroptosis. Anti-inflammatory exosomal ncRNAs exert synergistic effects: miR-146a targets TLR4/MyD88, miR-340-5p suppresses JAK2/STAT3, and miR-16-5p is sponged by circZFHX3 to upregu

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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