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Fig. 2 | Cell Communication and Signaling

Fig. 2

From: Exosomes: mediators regulating the phenotypic transition of vascular smooth muscle cells in atherosclerosis

Fig. 2

Multivesicular bodies are fused with the cytomembrane and exosomes are released. Exosomes promote the proliferation and migration of VSMCs through the miR-92a-3p/PTEN, miR-21-3p/PTEN/NF-kappaB, miRr-222, and lncRNA LIPCAR pathways, leading to intima hyperplasia. However, the TET2, miR-133, miR-143/145/KLF4/5, miR-663/JunB, and miR-155-5p/PKG1/NO/cGMP pathways improve the pathological process and vascular remodeling by inhibiting proliferation and migration of VSMCs. miR-106A/TIMP-2, circHIPK3/miR-106a-5p/Foxo1, and miR-26b/TGF-β/MAPK pathways promote apoptosis of VSMCs to promote a vascular inflammatory reaction and vascular rupture. miR-106a-3p binds CASP9 to inhibit the caspase pathway in VSMCs. miR-125b-5p downregulates Map4k4, and both inhibit VSMC apoptosis to reduce vascular stenosis and inflammation

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Cell Communication and Signaling

ISSN: 1478-811X