Retracted: Interleukin‐1 blockade treatment decreasing cardiovascular risk

Zheng, Zhou; Zeng, Xun; Nie, Xiao‐Ying; Cheng, Yun‐Jiu; Li, Jun; Lin, Xuemei; Yao, Hao; Ji, Chengcheng; Chen, Xumiao; Fan, Jia; Wu, Shuizhu

doi:10.1002/clc.23246

“…Our findings are consistent with a recent meta-analysis that studied the effect of IL-1 blockage on cardiovascular risk. The authors found an overall increased risk of recurrent MI with anakinra after pooling data from a total of five anakinra trials [ 47 ]. Although we only included three of the five trials based on our prespecified inclusion criteria (we excluded one study that included only the heart failure population and another study that did not have cardiovascular outcome as either primary or secondary end points) in our analysis, we found similar risk estimates with a wide confidence interval.…”

Section: Discussionmentioning

confidence: 99%

Comparative Effectiveness of Anti-Inflammatory Drug Treatments in Coronary Heart Disease Patients: A Systematic Review and Network Meta-Analysis

Wudexi

¹

,

Shokri

²

,

Abo-Aly

³

et al. 2021

Mediators of Inflammation

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Introduction and Hypothesis. The role of inflammation is widely recognized in the pathogenesis of coronary artery disease. Research on animal models had shown the potential benefits of targeting specific inflammatory pathways. However, studies on human subjects are limited with small number of patients and no head-to-head comparisons. Methods. We conducted a network meta-analysis of randomized controlled trials that studied the effects of anti-inflammatory medications on cardiovascular outcomes of coronary artery disease patients. We searched the electronic database until March 2020 for relevant studies. Results. Nineteen trials examining the efficacy of eight anti-inflammatory medications (pexelizumab, anakinra, colchicine, darapladib, varespladib, canakinumab, inclacumab, and losmapimod) were selected for analysis. Overall, there is no statistically significant difference in all-cause mortality, cardiovascular mortality, revascularization, and major cardio and cerebrovascular events (MACCE) with the use of anti-inflammatory drugs. However, we found the use of colchicine significantly reduces the odds of developing stroke by approximately 75% (OR 0.26, CI 0.10-0.63). Colchicine use was also associated with a lower risk of revascularization and MACCE compared to the other agents. Our subgroup analyses comparing the timing of medication initiation (within 7 days vs. >7 days) and clinical presentation (ACS vs. non-ACS) revealed a significant reduction in the risk of recurrent MI in the group that received medication after seven days (OR 0.92, CI 0.86-0.99) and the non-ACS group (OR 0.88, CI 0.80-0.98). Conclusion. Although many anti-inflammatory medications have failed to reduce adverse cardiovascular outcomes in the CAD population, selected medications show promise among subgroups of patients without ACS or after the first week following an acute ischemic event. Future studies examining the proper timing and targetable anti-inflammatory pathways are warranted.

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“…This study suggested that TMAO is negatively correlated with NO, therefore TMAO may cause atherosclerosis by reducing NO. IL-8 can stimulate the proliferation of vascular smooth muscle cells and accelerate the formation of atherosclerotic plaque [ 33 , 34 ]. In our study, we could not find atherosclerosis were related to IL-8, which may be due to relatively small sample size.…”

Section: Discussionmentioning

confidence: 99%

Positive Association of Plasma Trimethylamine-N-Oxide and Atherosclerosis in Patient with Acute Coronary Syndrome

Kong

¹

,

Ma

²

,

Chen

³

2022

Cardiovascular Therapeutics

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Aim. Atherosclerosis is the major cause of acute coronary syndrome (ACS) which is a significant contributor to both morbidity and mortality in the world. The microbiome-derived metabolite trimethylamine-N-oxide (TMAO) has aroused great interest and controversy as a risk factor of atherosclerosis. Therefore, in this study, we aimed at investigating whether plasma TMAO can be a risk factor of atherosclerosis in coronary artery of patients with ACS and how this relates to lipids and proinflammatory cytokines in plasma. Methods. We enrolled consecutive patients with ACS who underwent percutaneous coronary intervention (PCI). Gensini scoring was used to evaluate angiographic atherosclerosis in the coronary artery of the patients. 13 patients were divided into low ( Gensini score < 25 ), 33 into intermediate (Gensini score 25-50), and 81 into severe atherosclerosis (Gensini score ≥50). Plasma TMAO, vasculitis factors, and cardiovascular biomarkers were measured by clinical biochemistry, intima-media thickness (IMT) of carotid artery was determined by the Color Doppler ultrasound, and the atherosclerotic lesion in coronary artery was assessed in PCI. Results. Plasma TMAO concentrations were positively associated with Gensini score ( OR = 0.629 , p < 0.001 ) and Gensini subgroup ( R = 0.604 , p < 0.0 01). Plasma TMAO concentrations in patients with severe coronary atherosclerosis were higher than those of patients with moderate coronary atherosclerosis, and the plasma TMAO concentrations of patients with moderate coronary atherosclerosis were higher than those of patients with mild coronary atherosclerosis, the difference was statistically significant [4.73 (3.13, 4.62) versus 1.13 (0.63, 3.34) versus 0.79 (0.20, 1.29), p < 0.001 ], respectively. Furthermore, ROC analysis showed that plasma TMAO could identify the severity of atherosclerosis ( p < 0.001 ). The AUC of TMAO for severe atherosclerosis was 0.852 ( 95 % CI = 0.779 − 0.925 ). The sensitivity and specificity of TMAO for identifying severe atherosclerosis are 96.3% and 63.0% when the cut-off value of TMAO was set at 1.2715 pg/ml. Furthermore, logistic regression analysis showed plasma TMAO concentrations were positively associated with severity of atherosclerosis in coronary artery ( OR = 1.934 , 95 % CI = 1.522 − 2.459 , p < 0.001 ). For all that, negatively association was observed between TMAO and age ( OR = − 0.224 , p < 0.05 ), B-type natriuretic peptide (BNP) ( OR = − 0.175 , p < 0.05 ), and interleukin-8 (IL-8) ( OR = − 0.324 , p < 0.001 ), while positive association was observed between TMAO and nitric oxide (NO) ( OR = 0.234 , p < 0.01 ). However, there is no obvious association was observed between Gensini score and cardiovascular biomarkers, vasculitis factors, and carotid IMT, respectively. Conclusion. Our cross-sectional observation suggested that plasma TMAO concentrations positively associated with coronary atherosclerosis in ACS patients and serve as a risk factor for severe atherosclerosis. Plasma TMAO also correlated with age, BNP, IL-8, and NO. However, no obvious association was found between atherosclerosis with vasculitis factors and cardiovascular biomarkers in this study, and there was no conclusive evidence showing TMAO enhance atherosclerosis via regulation of inflammation or lipid.

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“…The IL-1 superfamily of cytokines also plays a vital role in immunity by regulating host defenses, inflammation, and injury. IL-1 inhibition improves glycemic control, and decreases the incidence of cardiovascular disease ( Herder et al, 2015 ; Zheng et al, 2019 ). Notably, IL-33, a cytokine from the IL-1 family, is an inflammatory mediator, that is, increased in OSA patients compared to controls ( Gabryelska et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Construction of a mitochondrial dysfunction related signature of diagnosed model to obstructive sleep apnea

Liu

¹

,

Hao²,

Li³

et al. 2022

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Background: The molecular mechanisms underlying obstructive sleep apnea (OSA) and its comorbidities may involve mitochondrial dysfunction. However, very little is known about the relationships between mitochondrial dysfunction-related genes and OSA.Methods: Mitochondrial dysfunction-related differentially expressed genes (DEGs) between OSA and control adipose tissue samples were identified using data from the Gene Expression Omnibus database and information on mitochondrial dysfunction-related genes from the GeneCards database. A mitochondrial dysfunction-related signature of diagnostic model was established using least absolute shrinkage and selection operator Cox regression and then verified. Additionally, consensus clustering algorithms were used to conduct an unsupervised cluster analysis. A protein–protein interaction network of the DEGs between the mitochondrial dysfunction-related clusters was constructed using STRING database and the hub genes were identified. Functional analyses, including Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, gene set enrichment analysis (GSEA), and gene set variation analysis (GSVA), were conducted to explore the mechanisms involved in mitochondrial dysfunction in OSA. Immune cell infiltration analyses were conducted using CIBERSORT and single-sample GSEA (ssGSEA).Results: we established mitochondrial dysfunction related four-gene signature of diagnostic model consisted of NPR3, PDIA3, SLPI, ERAP2, and which could easily distinguish between OSA patients and controls. In addition, based on mitochondrial dysfunction-related gene expression, we identified two clusters among all the samples and three clusters among the OSA samples. A total of 10 hub genes were selected from the PPI network of DEGs between the two mitochondrial dysfunction-related clusters. There were correlations between the 10 hub genes and the 4 diagnostic genes. Enrichment analyses suggested that autophagy, inflammation pathways, and immune pathways are crucial in mitochondrial dysfunction in OSA. Plasma cells and M0 and M1 macrophages were significantly different between the OSA and control samples, while several immune cell types, especially T cells (γ/δ T cells, natural killer T cells, regulatory T cells, and type 17 T helper cells), were significantly different among mitochondrial dysfunction-related clusters of OSA samples.Conclusion: A novel mitochondrial dysfunction-related four-gen signature of diagnostic model was built. The genes are potential biomarkers for OSA and may play important roles in the development of OSA complications.

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Retracted: Interleukin‐1 blockade treatment decreasing cardiovascular risk

Cited by 15 publications

References 32 publications

Comparative Effectiveness of Anti-Inflammatory Drug Treatments in Coronary Heart Disease Patients: A Systematic Review and Network Meta-Analysis

Comparative Effectiveness of Anti-Inflammatory Drug Treatments in Coronary Heart Disease Patients: A Systematic Review and Network Meta-Analysis

Positive Association of Plasma Trimethylamine-N-Oxide and Atherosclerosis in Patient with Acute Coronary Syndrome

Construction of a mitochondrial dysfunction related signature of diagnosed model to obstructive sleep apnea

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