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Review
. 2022 Oct 11;20(1):153.
doi: 10.1186/s12964-022-00949-6.

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

Jiali Yao  1 , Linqian Cai  1 , Yingrui Chen  1 , Jie Zhang  2 , Wenwen Zhuang  1 , Jingyan Liang  1   3 , Hongliang Li  4   5
Affiliations
Review

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

Jiali Yao et al. Cell Commun Signal. .

Abstract

Cardiovascular disease is one of the leading causes of human mortality worldwide, mainly due to atherosclerosis (AS), and the phenotypic transition of vascular smooth muscle cells (VSMCs) is a key event in the development of AS. Exosomes contain a variety of specific nucleic acids and proteins that mediate intercellular communication. The role of exosomes in AS has attracted attention. This review uses the VSMC phenotypic transition in AS as the entry point, introduces the effect of exosomes on AS from different perspectives, and discusses the status quo, deficiencies, and potential future directions in this field to provide new ideas for clinical research and treatment of AS. Video Abstract.

Keywords: Atherosclerosis; Exosomes; Phenotypic transition; Vascular smooth muscle cells.

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Conflict of interest statement

None declared.

Figures

Fig. 1
Fig. 1
The miR-29b, LncH19/Runx2, miR-34a/TGF-β, and miR-128-3p/Wnt pathways promote the osteoblast phenotype to increase plaque stability. The miR-133a/Runx2, miR-204/miRr-211/BMP2, miR-125b/Ets-1, miR-223-3p/IL-6/STAT3, and miR-146a/TXNIP pathways reduce vascular calcification and senescence by inhibiting the phenotypic transition from VSMCs to osteoblasts and inducing plaque rupture
Fig. 2
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
Fig. 3
Fig. 3
Macrophage-derived exosomal miR-155-5p and miR-221-5p promote EC proliferation to help vascular angiogenesis. EC-derived exosomal circRNA007793 inhibits miR-622 to promote cell aging. LINC01005 promotes proliferation and migration of VSMCs by regulating the miR-128-3p/KLF4 axis, while ACE2 down-regulates the activated NF-kappaB pathway to inhibit this process. Notch3 promotes the aging of VSMCs to ease vasosclerosis through the mTOR signaling pathway. VSMC-derived exosomal miR-155 inhibits EC proliferation to prevent damage to the vascular endothelium
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