Innovative Strategy for Enhanced Delivery of Anti-Fibrotic miR-150 via PDGFR-Targeted Exosomes for Fibrosis Treatment.

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)

Background Fibrosis, caused by hepatic stellate cell (HSC) activation and resulting in extracellular matrix accumulation, cirrhosis, and ultimately liver failure, remains a critical challenge. Recent advances in exosome-based drug delivery systems offer an innovative approach by specifically targeting activated HSCs to combat fibrotic diseases. This study evaluated the anti-fibrotic potential of miR-150-loaded exosomes engineered with platelet-derived growth factor receptor (PDGFR)-targeting peptides for precise delivery to activated HSCs. Methods Adipose-derived stem cells were genetically engineered to express PDGFR-targeting peptides via pDisplay vectors, resulting in the production of targeted exosomes (tEx). Subsequently, miR-150 was loaded into the targeted exosomes, termed tEx. In vitro and in vivo studies were conducted using a thioacetamide-induced liver fibrosis model. Results Either real-time polymerase chain reaction or western blot analysis demonstrated that tEx significantly reduced fibrotic markers, including alpha-smooth muscle actin, collagen type I alpha 1 chain, and transforming growth factor beta 1, both in vitro and in vivo. Western blotting showed a 40% decrease in collagen deposition, while enzyme-linked immunosorbent assay indicated a 30% reduction in serum liver enzyme levels (aspartate transaminase and alanine aminotransferase) compared to controls. Im

Evidence level

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

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