Cardiovascular diseases (CVDs) are the main cause of death among patients with type 2 diabetes mellitus (T2DM), particularly in low- and middle-income countries. To effectively prevent the development of CVDs in T2DM, considerable effort has been made to explore novel preventive approaches, individualized glycemic control and cardiovascular risk management (strict blood pressure and lipid control), together with recently developed glucose-lowering agents and lipid-lowering drugs. This review mainly addresses the important issues affecting the choice of antidiabetic agents and lipid, blood pressure and antiplatelet treatments considering the cardiovascular status of the patient. Finally, we also discuss the changes in therapy principles underlying CVDs in T2DM.

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Diabetic retinopathy (DR) is a common diabetic complication and the main cause of blindness worldwide, which seriously affects the quality of life of patients. Studies have shown that noncoding RNA (ncRNA) has distinct differentiated expression in DR and plays an important role in the occurrence and development of DR. ncRNAs represented by microRNAs (miRNAs), lncRNAs (lncRNAs), and circRNAs (circRNAs) have been shown to be widely involved in the regulation of gene expression and affect multiple biological processes of retinopathy. This article will review three RNAs related to the occurrence and development of DR on the basis of previous studies (especially their effects on retinal microangiopathy, retinal pigment epithelial cells, and retinal nerve cells) and discuss their underlying mechanisms and connections. Overall, this review will help us better understand the role of ncRNAs in the occurrence and development of DR and provide ideas for exploring potential therapeutic directions and targets.

Objective: To investigate the relationship between serum 25-hydroxyvitamin D [25(OH)D] levels and blood glucose and lipid levels in people over 18 years of age in Gansu, China. Subjects and Methods: A total of 1928 volunteers (958 males and 970 females) were selected. The prevalence of abnormal glucose metabolism and lipid metabolism in the vitamin D deficiency group (<20 ng/mL) and the non-vitamin D deficiency group (≥20 ng/mL) were compared. The correlations between serum 25(OH)D and blood glucose and lipid were analyzed. Results: A total of 1681 patients had 25(OH)D deficiency, with an overall prevalence of 87.2% (82.9% in males and 91.4% in females). The levels of 25(OH)D in the diabetic group and the IGT/IFG group were significantly lower than that in the normal group. The level of 25(OH)D was significantly lower in the dyslipidemia group than that in the normal group, and was significantly lower in the fasting plasma glucose (FPG) ≥5.6 mmol/L group than that in the FPG <5.6 mmol/L group (p=0.002). The 25(OH)D level in the serum triglyceride (TG) ≥1.7 mmol/L group was significantly lower than that of the TG <1.7 mmol/L group (p=0.0274). The age, heart rate, TG, TC, FPG and H 2 PG levels in the vitamin D deficiency group were significantly higher than those in the non-vitamin D deficiency group (p<0.05). The prevalence of FPG ≥5.6 mmol/L in the vitamin D deficiency group was higher than that in the non-vitamin D deficiency group (23.5% vs 16.6%, p=0.016). Multiple linear regression analysis suggested that serum 25(OH)D levels were independently correlated with gender, age, FPG, TG and heart rate (β=−0.218, −0.129, −0.075, β=−0.103, −0.058, all p<0.05). Conclusion: The incidences of dyslipidemia and dysglycemia were higher in the vitamin D deficiency group. The vitamin D level was independently and negatively correlated with FPG and TC, but not with waist circumference, BMI and blood pressure.

Bone metabolism is closely related to oxidative stress. As one of the core regulatory factors of oxidative stress, NRF2 itself and its regulation of oxidative stress are both involved in bone metabolism. NRF2 plays an important and controversial role in the regulation of bone homeostasis in osteoblasts, osteoclasts and other bone cells. The role of NRF2 in bone is complex and affected by several factors, such as its expression levels, age, sex, the presence of various physiological and pathological conditions, as well as its interaction with certains transcription factors that maintain the normal physiological function of the bone tissue. The properties of NRF2 agonists have protective effects on the survival of osteogenic cells, including osteoblasts, osteocytes and stem cells. Activation of NRF2 directly inhibits osteoclast differentiation by resisting oxidative stress. The effects of NRF2 inhibition and hyperactivation on animal skeleton are still controversial, the majority of the studies suggest that the presence of NRF2 is indispensable for the acquisition and maintenance of bone mass, as well as the protection of bone mass under various stress conditions. More studies show that hyperactivation of NRF2 may cause damage to bone formation, while moderate activation of NRF2 promotes increased bone mass. In addition, the effects of NRF2 on the bone phenotype are characterized by sexual dimorphism. The efficacy of NRF2-activated drugs for bone protection and maintenance has been verified in a large number of in vivo and in vitro studies. Additional research on the role of NRF2 in bone metabolism will provide novel targets for the etiology and treatment of osteoporosis.