Abstract
Aging is a progressive loss of physiological integrity and functionality process which increases susceptibility and mortality to diseases. Vascular aging is a specific type of organic aging. The structure and function changes of endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) are the main cause of vascular aging, which could influence the threshold, process, and severity of vascular related diseases. Accumulating evidences demonstrate that exosomes serve as novel intercellular information communicator between cell to cell by delivering variety biologically active cargos, especially exosomal non-coding RNAs (ncRNAs), which are associated with most of aging-related biological and functional disorders. In this review, we will summerize the emerging roles and mechanisms of exosomal ncRNAs in vascular aging and vascular aging related diseases, focusing on the role of exosomal miRNAs and lncRNAs in regulating the functions of ECs and VSMCs. Moreover, the relationship between the ECs and VSMCs linked by exosomes, the potential diagnostic and therapeutic application of exosomes in vascular aging and the clinical evaluation and treatment of vascular aging and vascular aging related diseases will also be discussed.
Highlights
Vascular aging is a specific type of organic aging, leading to major adverse cardiovascular events including restenosis, atherosclerosis, vascular calcification (VC) and pulmonary hypertension
A large number of studies dealing with circulating exosomes and their cargos prove that exosomal miRNAs and long noncoding RNAs (lncRNAs) were involved in regulating endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) dysfunction, which significantly affecting the process of vascular aging [12, 13]
MiR-126-3p enhanced VSMCs angiogenesis by suppressing the expression of its known target, SPRED1, simultaneously modulating the expression of genes involved in angiogenic pathways including vascular endothelial growth factor (VEGF), angiopoietin 1 (ANG1), angiopoietin 2 (ANG2), matrix metallopeptidase 9 (MMP9), thrombospondin 1 (TSP1) and so on [86]
Summary
Vascular aging is a specific type of organic aging, leading to major adverse cardiovascular events including restenosis, atherosclerosis, vascular calcification (VC) and pulmonary hypertension. 3; SOCS5: suppressor of cytokine signaling 5; RhoB: ras homologue family member B; Sp1: specificity protein 1; VEGF: vascular endothelial growth factor; NF-kB: nuclear factor-kappa B; EGFR epidermal growth factor receptor; BCL2: B-cell CLL/lymphoma 2; SIRT1: silent information regulator 1; ICAM-1: intercellular adhesion molecule-1; DLL4: delta-like 4; TRPM7: transient receptor potential melastatin 7; ANG2: Angiopoietin 2; IGF-1: insulinlike growth factor-1; Hsp: small heat-shock protein 20; Ets: E26 transformation-specific 2; PCNA: proliferating cell nuclear antigen; bFGF: basic fibroblast growth factor; IL-6: interleukin 6; TNF-α: tumor necrosis factor alpha; SAA3: serum amyloid antigen 3 ; TGFβ : transforming growth factor β. A large number of studies dealing with circulating exosomes and their cargos prove that exosomal miRNAs and lncRNAs were involved in regulating ECs and VSMCs dysfunction, which significantly affecting the process of vascular aging [12, 13]. In this review, we summarize the current knowledge about the exosomal ncRNAs focusing on the role of miRNAs and lncRNAs in vascular aging, especially targeting at the effects on ECs and VSMCs and the information communication between these cells
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