“…The main mechanisms of target organ damage by BPV are as follows:(1) inflammatory reaction [20] :When BPV increases, the abnormal longitudinal shear force and ring tension on the blood vessel wall and platelets increase, then promotes the endothelial injury and platelet activation, increases the synthesis and release of inflammatory factors, especially IL-6, promotes the occurrence of inflammatory reaction, and finally accelerates the occurrence and development of atherosclerosis; (2) The activation of renin-angiotensin-aldosterone (RAS) system damages cardiomyocytes [32]: increased blood pressure variability can cause the activation of RAS system, promote cardiomyocyte protein synthesis, DNA synthesis and cell apoptosis in myocardial fibroblasts and other mechanisms lead to ventricular remodeling and left ventricular function change; (3)Direct damage to endothelial cells [33]: either too high or too low blood pressure has adverse effects on the body, and the rapid decrease in blood pressure may lead to obvious or subclinical ischemic injury to the target organs, while the sudden increase in blood pressure can lead to capillary endothelial shear stress injury. Blood pressure variability is considered an independent predictor of early renal impairment [34], also a poor prognostic factor for the occurrence, progression, and severity of renal outcomes in patients undergoing CKD and hemodialysis [35]. Chronic kidney disease is also an important risk factor for cardiovascular disease, infection, and cognitive impairment [36].…”