## 3 Therapeutic Potential of Exosomes in Different Diseases
### Therapeutic Potential of Exosomes in Myocardial Diseases  
Exosomes play a crucial participatory role in the pathophysiological pathway of the cardiovascular system, and can become effective targets for clinical applications [63]. Vascular endothelial dysfunction is a critical primary mechanism at the onset of atherosclerosis (AS), and intercellular communication has been identified as a significant part of the pathological process [64; 65]. First, endothelial cells (ECs) can express vesicles, as well as absorbing vesicles derived from EC under oxidative pressure,reducing the production of nitric oxide (NO) that has a protective role [66]. Furthermore, it was observed in a previous study that endothelial microbes of coronary artery disease (CAD) were diffused in patients containing miR-92a-3p; a fine vesicle in selected CAD patients, largely controlled by vesicular performance and internal integrity [67]. Similarly, atherosclerotic stimuli as IL-6 or ox-LDL (oxidized low-density lipoprotein) that specifically enhance miR-92a-3p encapsulation in EMV, and EMVs mediated with EMV-3p eventually strengthen the vascular responses in targeted ECs through a THBS1-based mechanism (thrombospondin 1) [68]. Additionally, the information exchange between cracker and plaque cells involves the modification of the endothelial balance. In a previous study, for example, it was observed that AS endothelial apoptosis was caused by growth mass specificity following exosomal lncRNA GAS5 transfer from macrophages to ECs. Furthermore, endothelial apoptosis is initiated by exosomal lncRNA GAS5-overexpressing THP-1 cells while exosomal lncRNA GAS5 knockout cells inhibit this pathway [69]. Meanwhile, the kruppel-like factor 5 (KLF5) up-regulates ox-LDL in vascular smooth muscle cells (SMCs), resulting in endothelial dysfunction. Vascular remodeling is regulated by zinger fingers and KLF5, a known transcription factor. Studies have found that SMCs expressing KLF5 affect the endothelial functions by controlling multiple microRNAs. Of these multiple microRNAs, the most important of them is miR-155 (a known proinflammatory factor). The resulting exosomes produced by KLF5-overexpression SMCs are well enriched with miR-155. Poor barrier function and weak reproductive capacity are expressed by the ECs [70; 71]. Nevertheless, these effects can be prevented by miR-155 suppression or KLF5 disability. In addition, exosomes resulting from SMC (SMC-exos) enriched with miR-221/222 have been identified to interrupt autophagy of endothelial cells through the PTEN/Akt signaling mechanism making ECs more likely to stimulate atherosclerosis. Exosomes derived from platelets help to maintain the function of endothelial vasculature, but whether the modulatory effect is harmful or beneficial is still contested [72]. Some results suggest that the absorption of external platelets can lead to endothelial adhesion and programmed cell death, while others draw inconsistent conclusions [73]. For instance, platelet-exos enriched with miR-320 or miR-223 inhibited inflammation and EC mobility by reducing the appearance of ICAM-1 in EC recipients [74; 75]. The reason for the discrepancies is related to the complexity of the packed charges in the platelets, especially the ubiquitin/protease system found in the outer platelets that stimulate the degradation of the inflammatory substances [76; 77]. Exosomes from adipose-derived stem cells have been shown to express CD9 and CD29 proteins that protect cardiomyocytes during oxidative stress [22]. Furthermore, exosomes obtained from adipose tissue-derived Mesenchymal stem cells (ADMSCs) promoted cardiac function, particularly myocardium, by inhibiting cardiomyocytes apoptosis and promoting angiogenesis [32]. Finally, induced pluripotent stem cells (iPSCs) obtained from EVs ensure the cardioprotection of the cardiac cells with reference to the left ventricular function in vivo [33]. Prolonged cholesterol precipitation in macrophages leads to atheroma. Exosomes are believed to be incorporated in lipid modulation.