Extracellular vesicles (EVs) in ischemic conditioning and angiogenesis: Focus on endothelial derived EVs

Abstract

During myocardial ischemia, timely reperfusion is critical to limit infarct area and the overall loss of cardiac contractile function. However, reperfusion further exacerbates the damage of the ischemic heart. This type of injury is known as ischemia-reperfusion injury (IRI). Ischemic conditioning is a procedure which consists of brief cycles of ischemia and reperfusion in order to protect the myocardium against IRI. Remote ischemic conditioning (RIC), namely transient brief episodes of ischemia at a remote site before a subsequent damaging ischemia/ reperfusion procedure of the target organ (e.g., the heart), protects against IRI. However, how the stimulus of RIC is transduced from the remote organ to the ischemic heart is still unknown. Recently, extracellular vesicles (EVs) have been proposed to have a role in the RIC procedure. The endothelium releases EVs and is also one of the tissues mostly exposed to EVs during their journey to the target organ. Moreover, EVs may have important roles in angiogenesis and, therefore, in the remodeling of post-ischemic organs. Here we analyze how EVs may contribute to the overall cardioprotective effect and the implication of the endothelium and its EVs in RIC mediated acute cardioprotection as well as in angiogenesis.

Therapeutic Applications of Extracellular Vesicles for Myocardial Repair

“…EVs are involved in the process of cardiovascular pathology, the communication between cardiomyocytes, fibroblasts, smooth muscle cells and endothelial cells, and the regulation of cardiac regeneration, ventricular remodeling and angiogenesis ( 22 – 24 ). Cardiomyocytes are the main cells of the heart and their EVs play different roles in myocardial repair ( 25 ).…”

Lymphatic and Blood Endothelial Extracellular Vesicles: A Story Yet to Be Written

“…Beside cardioprotective miR-126 and miR-199a [ 61 ] and pro-proliferative miR-25, miR-186, and miR-221 [ 71 ], BEC-EVs transfer a plethora of further miRNAs, yRNA fragments [ 71 ], and lncRNAs [ 73 ]. Cardioprotective EV properties could be hampered by caveolin-1 exosomes from interleukin-3 (IL-3)-stimulated BECs [ 74 ]. In vitro, EC morphology also regulates inflammatory response, as EVs from elongated BECs carry markedly higher amounts of anti-inflammatory miR-10a [ 75 ].…”

Old and New Biomarkers Associated with Endothelial Dysfunction in Chronic Hyperglycemia

“…In addition, some studies have suggested that EEVs carry messages which may influence endothelial cells' reaction to atherogenic insults. Therefore, they could be considered a novel target for the modulation of CVD progression [ 44 , 45 ]. The paucity of studies and their heterogeneity do not allow to draw clear conclusions on this intriguing hypothesis.…”