Hypoxic hypoxia, including abnormally low partial pressure of inhaled oxygen, external respiratory dysfunction‐induced respiratory hypoxia and venous blood flow into the arterial blood, is characterized by decreased arterial oxygen partial pressure, resulting in tissue oxygen deficiency. The specific characteristics include reduced arterial oxygen partial pressure and oxygen content. Hypoxic hypoxia diseases (HHDs) have attracted increased attention due to their high morbidity and mortality and mounting evidence showing that hypoxia‐induced oxidative stress, coagulation, inflammation and angiogenesis play extremely important roles in the physiological and pathological processes of HHDs‐related vascular endothelial injury. Interestingly, endothelial microvesicles (EMVs), which can be induced by hypoxia, hypoxia‐induced oxidative stress, coagulation and inflammation in HHDs, have emerged as key mediators of intercellular communication and cellular functions. EMVs shed from activated or apoptotic endothelial cells (ECs) reflect the degree of ECs damage, and elevated EMVs levels are present in several HHDs, including obstructive sleep apnoea syndrome and chronic obstructive pulmonary disease. Furthermore, EMVs have procoagulant, proinflammatory and angiogenic functions that affect the pathological processes of HHDs. This review summarizes the emerging roles of EMVs in the diagnosis, staging, treatment and clinical prognosis of HHDs.

Endothelial microvesicles (EMVs), released after endothelial cell (EC) apoptosis or activation, may carry many adverse signals and propagate injury by intercellular transmission. Caveolae are 50–100 nm cell surface plasma membrane invaginations involved in many pathophysiological processes. Recent evidence has indicated EMVs and caveolae may have functional effects in cells undergoing H/R injury. Propofol, a widely used anaesthetic, confers antioxidative stress capability in the same process. But the connection between EMVs, H/R, and caveolae remains largely unclear. Here, we found that H/R significantly increased the release of EMVs, the expression of CAV-1 (the structural protein responsible for maintaining the shape of caveolae), oxidative stress, and the mitochondrial damage, and all these changes were inhibited by propofol preconditioning. Interestingly, the caveolae inhibitor Mβ-CD strengthened the protective effect of propofol preconditioning. We further found that the release of EMVs is more significantly reduced under propofol preconditioning in the presence of the caveolae inhibitor Mβ-CD. EMVs released from H/R-treated cells caused a substantially increased mitochondrial and cellular damage to normal HUVECs after 4 hours of coculture. Thus, we conclude that inhibition of caveolae contributes to propofol preconditioning-suppressed microvesicles release and cell injury by H/R.