Background MicroRNAs (miRNAs) have been shown to play a crucial role in inflammation regulation; however, their relationship with inflammation in acute gouty arthritis has not been fully elucidated. Herein, we conducted a study to explore the regulatory roles of miR‐223‐3p and miR‐22‐3p in gouty‐associated inflammation. Methods In vitro and in vivo experiments were conducted to examine the molecular mechanisms of miRNA regulation in gouty inflammation. Dual‐luciferase reporter assay was used to verify the direct target of miR‐223‐3p and miR‐22‐3p. Results We found that miR‐223‐3p and miR‐22‐3p interacted with the 3′ untranslated region segment of NLRP3 (nucleotide‐binding domain leucine‐rich repeat [NLR] and pyrin domain containing receptor 3) and inhibited its expression. A decreased expression of miR‐223‐3p and miR‐22‐3p was observed in both mice air pouch synovium and phorbol myristrate acetate‐treated THP‐1 cells stimulated with monosodium urate (P < .05). Compared with the negative control group, NLRP3 expression at the transcript and protein level in miR‐223‐3p and miR‐22‐3p overexpression group significantly decreased after 6 hours of monosodium urate treatment in vivo and in vitro (P < .05). The results of the dual‐luciferase reporter assay demonstrated that miR‐223‐3p and miR‐22‐3p directly targeted NLRP3. Conclusion The findings of the present study show that miR‐223‐3p and miR‐22‐3p can reduce the inflammatory effects of gout by inhibiting the expression of NLRP3.
Diabetic kidney disease (DKD) is a common cause of end-stage renal disease, and diagnosis and treatment in time can help delay its progress. At present, there are more and more studies on the pathogenesis of DKD; mitochondrial dysfunction plays an important role in DKD. The occurrence and development of DKD is closely related to epigenetic changes and the interaction between mtDNA, ROS, inflammatory factors, and endothelial damage, which continuously aggravates kidney. The change of mtDNA is both the cause of DKD and the result of DKD. It is of great significance to incorporate the change of mtDNA into the monitoring of patients with diabetes. Existing evidence indicates that changes in mtDNA copy number in blood and urine reflect mitochondrial dysfunction and the severity of DKD. However, large-scale, long-term follow-up clinical trials are still needed to determine the threshold range. By the time, mitochondrial-targeted antioxidants will become a new method for the treatment of DKD and other diabetic complications; mtDNA also can be a therapeutic target for them.
Aims/Introduction To investigate the associations between parathyroid hormone (PTH) and non‐proliferative diabetic retinopathy (NPDR) in patients with type 2 diabetes mellitus. Materials and Methods Data were collected from 2,322 patients with type 2 diabetes mellitus in hospital between 2017 and 2019. The odds ratio (OR) and the corresponding 95% confidence interval related to the quartiles of PTH were obtained by logistic regression analysis after adjusting the potential confounding variation. Results The patients were stratified into quartiles (Q1–Q4) based on the PTH levels, with the cut‐off limits of ≤23.74, 23.74–29.47, 29.47–37.30 and >37.30 pg/mL in men, and ≤24.47, 24.47–31.22, 31.22–39.49 and >39.49 pg/mL in women. The first quartile (Q1) represents the lowest quartile and the fourth quartile (Q4) is the highest. According to the quartiles (Q1–Q4), the prevalence rate of NPDR in patients showed a significantly decreasing trend (37.9%, 36.3%, 34.0% vs 24.0% in men; 43.2%, 40.5%, 31.1% vs 26.2% in women, both P < 0.05). Independent of age, diabetes duration and other metabolic factors, multivariate logistic regression showed that participants in Q4 had a lower OR of NPDR than those in Q1 (OR 0.443, 95% confidence interval 0.300–0.654, P < 0.001 for men; OR 0.428, 95% confidence interval 0.283–0.646, P < 0.001 for women). Conclusions Low serum PTH levels were significantly associated with complications of NPDR in inpatients. Its causality remains to be further studied.
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