Objective. Obstructive sleep apnea syndrome (OSA) is the most common type of sleep disorders. This study aimed to systematically review the correlation between OSA and the risk of coronary atherosclerosis. Methods. Literature on case-control studies on the relationship between coronary heart disease (CHD) and sleep apnea syndrome was collected and collated, and the incidence of SAS in CHD and non-CHD patients was observed and compared. RevMan 5.2 analysis software and Stata12SE analysis software were used for heterogeneity test and combination analysis of the included studies. The results were expressed with odds ratio (OR), 95% confidence intervals (CI) were calculated, and publication bias and sensitivity tests were evaluated. Results. There was a statistical difference in OSA associated with the risk of coronary atherosclerosis between the experimental group and the control group [ OR = 1.38 , 95% CI (1.18, 1.62), P < 0.0001 , I 2 = 0 % , Z = 3.93 ]. OSA associated with vascular endothelial injury [ OR = 3.59 , 95% CI (3.00, 4.29), P < 0.00001 , I 2 = 90 % , Z = 14.09 ]. OSA is associated with vascular oxidation emergency [ OR = 2.19 , 95% CI (2.05, 2.33), P < 0.00001 , I 2 = 94 % , Z = 23.40 ]; OSA is associated with chronic vascular inflammation [ OR = 1.70 , 95% CI (1.39, 2.07), P < 0.00001 , I 2 = 16 % , Z = 5.18 ]. Conclusion. The incidence of obstructive sleep apnea in patients with CHD was higher than that in non-CHD patients, and obstructive sleep apnea was a risk factor for CHD.
Diffuse alveolar haemorrhage (DAH) is a rapidly developing condition owing to a lack of effective treatment and resulting in a high mortality rate in systemic lupus erythematosus (SLE). Neutrophil extracellular traps (NETs) contain numerous antigens and proinflammatory substances that directly damage the vascular endothelium and aggravate vascular inflammation, which is considered an important pathogenic factor of DAH in SLE. Therefore, blocking the release of NETs from neutrophils is an important target for the treatment of DAH in SLE. In this study, we investigated whether the inhibition of neutrophils releasing NETs could relieve DAH in SLE. Necrostatin-1 (Nec-1), a small molecule, has been reported to inhibit the release of NETs by neutrophils. In vitro experiments revealed that Nec-1 inhibited alveolar epithelial cell damage by preventing the release of NETs. Furthermore, vivo studies showed that Nec-1 alleviated lupus pulmonary haemorrhage in mice by reducing lung pathology severity, body weight, and serum inflammatory cytokine levels. Mechanistically, Nec-1 prevented NET release by inhibiting neutrophil elastase (NE) activation and N-Gasdermin D (N-GSDMD) expression. Additionally, immunohistochemistry and immunofluorescence findings showed that Nec-1 decreased NE expression in the lung tissues of mice with lupus pulmonary haemorrhage. Thus, NETs released by neutrophils contributed to the pathogenesis of DAH in SLE, and Nec-1 showed protective effects by the inhibition of NET production via the reduction of NE activation and N-GSDMD expression.
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