Hypertension is one of the most important risk factors for coronary heart disease (CHD). The regulation of blood pressure plays a significant role in the development and prognosis of CHD. Blood pressure variability (BPV) refers to the degree of fluctuation of blood pressure over a period of time and is an important indicator of blood pressure stability. Blood pressure fluctuations are complex physiological phenomena, being affected by physiological and pharmacological effects and regulated by behavioral, environmental, hydrodynamic, and neural factors. According to the different time periods for measuring BPV, it can be divided into very short-term, short-term, mid-term, and long-term. Multiple cardiovascular disease animal models and clinical experiments have consistently indicated that abnormal BPV is closely related to coronary events and is a risk factor for CHD independently of average blood pressure. Thrombosis secondary to plaque rupture (PR) or plaque erosion can cause varying blood flow impairment, which is the main pathological basis of CHD. Plaque morphology and composition can influence the clinical outcome, treatment, and prognosis of patients with CHD. Research has shown that PR is more easily induced by hypertension. After adjusting for the traditional factors associated with plaque development, in recent years, some new discoveries have been made on the influence of abnormal BPV on the morphology and composition of coronary plaques and related mechanisms, including inflammation and hemodynamics. This article reviews the impact of BPV on coronary plaques and their related mechanisms, with a view to prevent the occurrence and development of CHD by controlling BPV and to provide new prevention and treatment strategies for the clinical treatment of abnormal blood pressure.
Fibroblast growth factor-21 (FGF-21) performs a wide range of biological functions in organisms. Here, we report for the first time that FGF-21 suppresses thrombus formation with no notable risk of bleeding. Prophylactic and therapeutic administration of FGF-21 significantly improved the degree of vascular stenosis and reduced the thrombus area, volume and burden. We determined the antithrombotic mechanism of FGF-21, demonstrating that FGF-21 exhibits an anticoagulant effect by inhibiting the expression and activity of factor VII (FVII). FGF-21 exerts an antiplatelet effect by inhibiting platelet activation. FGF-21 enhances fibrinolysis by promoting tissue plasminogen activator (tPA) expression and activation, while inhibiting plasminogen activator inhibitor 1 (PAI-1) expression and activation. We further found that FGF-21 mediated the expression and activation of tPA and PAI-1 by regulating the ERK1/2 and TGF-β/Smad2 pathways, respectively. In addition, we found that FGF-21 inhibits the expression of inflammatory factors in thrombosis by regulating the NF-κB pathway.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.