Objective:To evaluate the efficacy and safety of allopurinol in the treatment of chronic kidney disease.Methods:The databases of Embase, PubMed and the Cochrane library were searched for randomized controlled trials of allopurinol in patients with chronic kidney disease. According to the Cochrane system evaluation method, two evaluators independently screened the literature and extracted the data, and analyzed the results with Revman 5.3 software.Results:Finally, 10 articles were included, including 940 patients (472 in the experimental group and 468 in the control group). Meta analysis showed that allopurinol treatment could reduce blood uric acid ( MD=-2.40, 95% CI: -2.74--2.05, P<0.01), 24-hour urinary protein ( MD=-0.61, 95% CI: -1.17--0.06, P=0.03) and increase estimation of glomerular filtration rate(eGFR) ( MD=2.51, 95% CI: 1.86-3.17, P<0.01). There was no significant difference in adverse events between the experimental group and the control group ( OR=1.40, 95% CI: 0.61-3.19, P=0.42), but allopurinol treatment could reduce the risk of cardiovascular events ( OR=0.58, 95% CI: 0.38-0.89, P=0.01). Conclusions:Allopurinol treatment of chronic kidney disease can reduce urinary protein, improve eGFR, and reduce the risk of cardiovascular events.

Long-chain acyl-coenzyme A (CoA) synthase 4 (ACSL4) is an enzyme that esterifies CoA into specific polyunsaturated fatty acids, such as arachidonic acid and adrenic acid. Based on accumulated evidence, the ACSL4-catalyzed biosynthesis of arachidonoyl-CoA contributes to the execution of ferroptosis by triggering phospholipid peroxidation. Ferroptosis is a type of programmed cell death caused by iron-dependent peroxidation of lipids; ACSL4 and glutathione peroxidase 4 positively and negatively regulate ferroptosis, respectively. In addition, ACSL4 is an essential regulator of fatty acid (FA) metabolism. ACSL4 remodels the phospholipid composition of cell membranes, regulates steroidogenesis, and balances eicosanoid biosynthesis. In addition, ACSL4-mediated metabolic reprogramming and antitumor immunity have attracted much attention in cancer biology. Because it facilitates the cross-talk between ferroptosis and FA metabolism, ACSL4 is also a research hotspot in metabolic diseases and ischemia/reperfusion injuries. In this review, we focus on the structure, biological function, and unique role of ASCL4 in various human diseases. Finally, we propose that ACSL4 might be a potential therapeutic target.
Humans ; Ferroptosis ; Apoptosis ; Phospholipids/metabolism* ; Nitric Oxide Synthase