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Abstract Objective Little is known about the magnitude of the relation of ambient fine particulate matter (PM2.5) constituents with hyperuricemia and serum uric acid (SUA) levels. Therefore, we aimed to assess the associations and to identify the most hazardous constituent. Methods This study included 72,840 participants from the China Multi-Ethnic Cohort. Annual average concentrations of PM2.5 mass and its major 7 constituents were matched to individuals by residential address. SUA levels exceeding 7.0 mg/dL (417 μmol/L) for men and 6.0 mg/dL (357 μmol/L) for women were considered to be hyperuricemia. Multiple logistic and linear regressions were performed on the association of single exposure to PM2.5 constituents with hyperuricemia and SUA, separately. The weighted quantile sum method was applied to examine the joint effect of PM2.5 constituents on hyperuricemia/SUA. Results Significant positive associations were discovered between PM2.5 constituents and SUA/hyperuricemia. For example, the odds ratio (95% confidence interval) of hyperuricemia for per standard deviation increase of PM2.5 mass, black carbon, organic matter, ammonium, and nitrate concentrations were 1.22 (1.12–1.32), 1.17 (1.08–1.27), 1.20 (1.10–1.31), 1.21 (1.11–1.31), and 1.28 (1.18–1.40), respectively. The joint exposure to PM2.5 constituents was significantly positively correlated with hyperuricemia (1.09, 1.05–1.14) and SUA (1.05, 1.03–1.06). And the weight of nitrate was the largest (0.668 for hyperuricemia, 0.586 for SUA). Conclusions Our findings suggest that long-term exposure to PM2.5 constituents is associated with increased SUA levels and a higher risk of hyperuricemia. In particular, nitrate seems to be the main contributor. This study may help prevent hyperuricemia by promoting the introduction of precise preventive measures. Graphical Abstract

Diabetes mellitus is a metabolic disease that is characterized by chronic hyperglycemia due to a variety of etiological factors. Long-term metabolic stress induces harmful inflammation leading to chronic complications, mainly diabetic ophthalmopathy, diabetic cardiovascular complications and diabetic nephropathy. With diabetes complications being one of the leading causes of disability and death, the use of anti-inflammatories in combination therapy for diabetes is increasing. There has been increasing interest in targeting significant regulators of the inflammatory pathway, notably receptor-interacting serine/threonine-kinase-1 (RIPK1) and receptor-interacting serine/threonine-kinase-3 (RIPK3), as drug targets for managing inflammation in treating diabetes complications. In this review, we aim to provide an up-to-date summary of current research on the mechanism of action and drug development of RIPK1 and RIPK3, which are pivotal in chronic inflammation and immunity, in relation to diabetic complications which may be benefit for explicating the potential of selective RIPK1 and RIPK3 inhibitors as anti-inflammatory therapeutic agents for diabetic complications.

Background: Exposure to particulate matter with aerodynamic diameters less than 2.5 µm (PM2.5) may increase the risk of 10-year atherosclerotic cardiovascular disease (ASCVD) risk. While PM2.5 is comprised of various components, the evidence on the correlation of its components with 10-year ASCVD risk and which component contributes most remains limited. Methods: Data were derived from the baseline assessments of China Multi-Ethnic Cohort (CMEC). In total, 69,722 individuals aged 35–74 years were included into this study. The annual average concentration of PM2.5 and its components (black carbon, ammonium, nitrate, sulfate, organic matter, soil particles, and sea salt) were estimated by satellite remote sensing and chemical transport models. The ASCVD risk of individuals was calculated by the equations from the China-PAR Project (prediction for ASCVD risk in China). The relationship between single exposure to PM2.5 and its components and predicted 10-year ASCVD risk was assessed using the logistic regression model. The effect of joint exposure was estimated, and the most significant contributor was identified using the weighted quantile sum approach. Results: Totally 69,722 participants were included, of which 95.8 % and 4.2 % had low and high 10-year ASCVD risk, respectively. Per standard deviation increases in the 3-year average concentration of PM2.5 mass (odds ratio [OR] 1.23, 95 % confidence interval [CI]: 1.12–1.35), black carbon (1.21, 1.11–1.33), ammonium (1.21, 1.10–1.32), nitrate (1.25, 1.14–1.38), organic matter (1.29, 1.18–1.42), sulfate (1.17, 1.07–1.28), and soil particles (1.15, 1.04–1.26) were related to high 10-year ASCVD risk. The overall effect (1.19, 1.11–1.28) of the PM2.5 components was positively associated with 10-year ASCVD risk, and organic matter had the most contribution to this relationship. Female participants were more significantly impacted by PM2.5, black carbon, ammonium, nitrate, organic matter, sulfate, and soil particles compared to others. Conclusion: Long-term exposure to PM2.5 mass, black carbon, ammonium, nitrate, organic matter, sulfate, and soil particles were positively associated with high 10-year ASCVD risk, while sea salt exhibited a protective effect. Moreover, the organic matter might take primary responsibility for the relationship between PM2.5 and 10-year ASCVD risk. Females were more susceptible to the adverse effect.

Diabetic nephropathy (DN) and diabetic retinopathy (DR) are the most serious and common diabetes-associated complications. DN and DR are all highly prevalent and dangerous global diseases, but the underlying mechanism remains to be elucidated. Ferroptosis, a relatively recently described type of cell death, has been confirmed to be involved in the occurrence and development of various diabetic complications. The disturbance of cellular iron metabolism directly triggers ferroptosis, and abnormal iron metabolism is closely related to diabetes. However, the molecular mechanism underlying the role of ferroptosis in DN and DR is still unclear, and needs further study. In this review article, we summarize and evaluate the mechanism of ferroptosis and its role and progress in DN and DR, it provides new ideas for the diagnosis and treatment of DN and DR.