Purine metabolism in the circulatory system yields uric acid as its final oxidation product, which is believed to be linked to the development of gout and kidney stones. Hyperuricemia is closely correlated with cardiovascular disease, metabolic syndrome, and chronic kidney disease, as attested by the epidemiological and empirical research. In this review, we summarize the recent knowledge about hyperuricemia, with a special focus on its physiology, epidemiology, and correlation with cardiovascular disease. This review also discusses the possible positive effects of treatment to reduce urate levels in patients with cardiovascular disease and hyperuricemia, which may lead to an improved clinical treatment plan.

Background Lipoprotein (a) is a determined causal risk factor for residual risks of recurrent ischemic cardiovascular events. Alirocumab has been found to reduce lipoprotein (a) levels. However, its effects on lipoprotein (a) and inflammation marker in a Chinese population with unstable angina remain to be characterized. Aim We aimed to assess the effect of alirocumab on lipoprotein (a) and inflammatory marker in Chinese subjects with unstable angina. Method In a retrospective before-after study, lipoprotein (a), interleukin-6 and other lipid profiles were measured before and after 4 weeks of alirocumab treatment in 53 patients with unstable angina (UA) who had already received oral lipid-lowering therapies. Results The alirocumab significantly lowered the levels of lipoprotein (a) (−11.28 mg/dL; p< 0.001) and interleukin-6 (-1.65 pg/mL; p < 0.001) after treatment. Moreover, there was a positive linear correlation between lipoprotein (a) and interleukin-6 at baseline (R=0.86; p < 0.001). Furthermore, in 11 patients with lipoprotein (a) levels ≥ 50 mg/dL at baseline, lipoprotein (a) (-27.37 mg/dL; p < 0.001) and interleukin-6 (-2.97 pg/mL; p < 0.001) decreased after treatment. In 42 patients with lipoprotein (a) levels < 50 mg/dL at baseline, lipoprotein (a) (-7.07 mg/dL; p = 0.001) and interleukin-6 (-1.31pg/mL, p < 0.001) also decreased after treatment. Conclusions Early application of alirocumab may be effective in reducing the levels of lipoprotein (a) and interleukin-6 in Chinese patients with unstable angina in the short term, especially in patients with lipoprotein (a) ≥ 50 mg/dL.

Background. Abdominal aortic aneurysm (AAA) is a fatal disease characterized by high morbidity and mortality in old population. Globally, effective drugs for AAA are still limited. Si-Miao-Yong-An decoction (SMYAD), a traditional Chinese medicine (TCM) formula with a high medical value, was reported to be successfully used in an old AAA patient. Thus, we reason that SMYAD may serve as a potential anti-AAA regime. Objective. The exact effects and detailed mechanisms of SMYAD on AAA were explored by using the experimental study and bioinformatics analysis. Methods. Firstly, C57BL/6N mice induced by Bap and Ang II were utilized to reproduce the AAA model, and the effects of SMYAD were systematically assessed according to histology, immunohistochemistry, and enzyme-linked immunosorbent assay (ELISA). Then, network pharmacology was applied to identify the biological processes, pathways, and hub targets of SMYAD against AAA; moreover, molecular docking was utilized to identify the binding ability and action targets. Results. In an animal experiment, SMYAD was found to effectively alleviate the degree of pathological expansion of abdominal aorta and reduce the incidence of Bap/Ang II-induced AAA, along with reducing the damage to elastic lamella, attenuating infiltration of macrophage, and lowering the circulating IL-6 level corresponding to the animal study, and network pharmacology revealed the detailed mechanisms of SMYAD on AAA that were related to pathways of inflammatory response, defense response, apoptotic, cell migration and adhesion, and reactive oxygen species metabolic process. Then, seven targets, IL-6, TNF, HSP90AA1, RELA, PTGS2, ESR1, and MMP9, were identified as hub targets of SMYAD against AAA. Furthermore, molecular docking verification revealed that the active compounds of SMYAD had good binding ability and clear binding site with core targets related to AAA formation. Conclusion. SMYAD can suppress AAA development through multicompound, multitarget, and multipathway, which provides a research direction for further study.