Neutrophil Extracellular Traps (NETs) are neutrophil-derived extracellular scaffolds, which typically consist of fibrous decondensed chromatins decorated with histones and granule proteins. Initially discovered as a host defence mechanism of neutrophil against pathogens, they have also been implicated in the progression of sterile inflammation-associated diseases such as autoimmune disease, diabetes, and cancer. In this review, we highlight and discuss the more recent studies on the roles of NETs in cancer development, with a special focus on cancer metastasis. Moreover, we present the strategies for targeting NETs in pre-clinical models, but also the challenging questions that need to be answered in the field.

Objective: This study aimed to examine the effects of low-dose statins on blood pressure in individuals diagnosed with prehypertension and borderline elevated blood lipids. Methods: From January 2020 to June 2021, a cohort of 150 patients with prehypertension and borderline elevated blood lipids was recruited from the Kangqiao Community Health Service Center, Pudong New Area, Shanghai. Participants were randomly divided into an experimental group and a control group, each comprising 75 patients. Both groups received standard lifestyle interventions. Additionally, the experimental group was treated with low-dose statins, while the control group was given with placebo. The treatment duration was three months. Blood pressure (systolic blood pressure (SBP), diastolic blood pressure (DBP)), blood lipids (total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C)), vascular endothelial function (nitric oxide (NO), endothelin-1 (ET-1), flow-mediated dilation (FMD)), and carotid intima-media thickness (IMT) were measured. These parameters were assessed at baseline, one month into treatment, and at the end of the three-month treatment period. Subsequently, patients were followed for two years to evaluate the incidence of hypertension. Results: Both SBP and DBP showed a progressive decrease from baseline to three months in both the experimental group and control group, with the experimental group experiencing a more significant reduction. Statistically significant differences were observed between the two groups, over time, and in group-by-time interactions (P < 0.05). Similarly, reductions in TC, TG, and LDL-C were more pronounced in the experimental group, with significant differences between the two groups, time points, and group-by-time interactions (P < 0.05). Improvements in NO and FMD levels and reductions in ET-1 levels were more marked in the experimental group, with statistically significant differences (P < 0.05). IMT reduction was also more notable in the experimental group, with significant differences between groups, over time, and in group-by-time interactions (P < 0.05). After two years of follow-up, the experimental group had a lower prevalence of hypertension compared to the control group (P <0.05). Conclusion: Low-dose statin therapy could effectively lower blood pressure and blood lipid levels, enhance vascular endothelial function, delay arteriosclerosis progression, and reduce the incidence of hypertension in patients with prehypertension and borderline elevated blood lipids.

Type 2 diabetes mellitus (T2DM) is a complex metabolic disorder. The nutritional status of vitamin D, an essential micronutrient, is closely linked to the onset and progression of T2DM. A growing body of research has shown that gut microbiota and its metabolites are emerging as a biological link connecting vitamin D and systemic glucose metabolism. Gut dysbiosis is prevalent in T2DM patients, which is characterized by reduced gut microbial diversity, increased abundance of pathogenic bacteria, and abnormal production of key metabolites such as short-chain fatty acids, bile acids and tryptophan derivatives. These abnormal changes in gut microecology and metabolites can impair intestinal barrier integrity and induce chronic low-grade inflammation in the body, and vitamin D deficiency may further exacerbate these abnormal processes. The evidence suggests that the regulatory effect of vitamin D on systemic glucose metabolism may be partially achieved through gut microbiota-related pathways. This review aims to explore whether, and by what mechanisms, the gut microbiota mediates the regulatory effect of vitamin D on T2DM. It also intends to conduct an analysis of the potential molecular mechanisms underlying the interactions between vitamin D, gut microbiota and T2DM, so as to provide a new theoretical basis and research ideas for the prevention and intervention of T2DM.