Exosomal MicroRNAs in Endothelial Repair: A Review of Molecular Mechanisms
Year: 2026
Type: article
Abstract: Background: The vascular endothelium regulates vascular permeability, haemostasis, vascular tone and inflammatory responses. Endothelial injury compromises vascular homeostasis and contributes to cardiovascular and metabolic disorders. Exosomes mediate intercellular communication by transporting bioactive molecules, including microRNAs (miRNAs), to recipient cells. Aim: This review examines the molecular mechanisms through which exosomal miRNAs may contribute to endothelial repair and restoration of vascular homeostasis. Methods: A narrative review of literature concerning exosomes, miRNAs, endothelial injury and repair, angiogenesis, inflammation and oxidative stress was undertaken. The evidence was synthesised thematically according to the cellular responses and signalling pathways described. Results: Exosomal miRNAs are associated with processes relevant to endothelial recovery, including migration, proliferation, angiogenesis, apoptosis, inflammation and oxidative stress. The reviewed evidence describes roles for miR-21, miR-126, miR-125b, miR-146a, miR-182-5p, miR-25-3p and miR-210. Their reported molecular targets and signalling pathways include PI3K/Akt, MAPK/ERK and NF-κB, as well as regulators of endothelial survival, inflammatory responses and vascular growth. These mechanisms may contribute to re-endothelialisation, recovery of barrier integrity and improved vascular function. However, the direction and extent of these effects depend on the cellular source, miRNA cargo and injury context. Conclusion: Exosomal miRNAs represent potential modulators of endothelial repair and candidates for biomarker and therapeutic investigation. Further work is needed to establish cell-specific effects, improve vesicle isolation and characterisation, clarify delivery mechanisms and assess clinical applicability.
Institution: Usmanu Danfodiyo University
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: diamond
OpenAlex ID: W7224477287