Cellular Crosstalk in the Vascular Wall Microenvironment: The Role of Exosomes in Vascular Calcification

Abstract

Vascular calcification is prevalent in aging, diabetes, chronic kidney disease, cardiovascular disease, and certain genetic disorders. However, the pathogenesis of vascular calcification is not well-understood. It has been progressively recognized that vascular calcification depends on the bidirectional interactions between vascular cells and their microenvironment. Exosomes are an essential bridge to mediate crosstalk between cells and organisms, and thus they have attracted increased research attention in recent years. Accumulating evidence has indicated that exosomes play an important role in cardiovascular disease, especially in vascular calcification. In this review, we introduce vascular biology and focus on the crosstalk between the different vessel layers and how their interplay controls the process of vascular calcification.

Keywords: endothelial cells; exosomes; immune cells; vascular calcification; vascular smooth muscle cells.

Figure 1

Diagram of the cell populations in the vascular microenvironment and their roles in vascular calcification. Endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) can induce phenotype transitions (EndMT, endothelial- mesenchymal transitions, a specific transition of ECs) in the microvasculature mineralization process via several signaling pathways. Adventitial fibroblasts could function in vascular calcification as well as vascular injury repair.

Figure 2

Exosome-mediated crosstalk in the vascular microenvironment. The exosomes derived from different cell populations can facilitate or inhibit vascular calcification via exosome-mediated crosstalk between VSMCs and other cell populations through different molecules, such as miRNAs and bone morphogenetic protein-2 (BMP-2), among others.