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The toll-like receptor 4 (TLR4), predominantly known for its role as an important mediator of immune reactions, is expressed in atherosclerotic lesions. Atherosclerosis resulting in cerebral or carotid arterial stenosis/occlusion plays the most important role in the occurrence of cerebral infarction (CI), and thus TLR4 polymorphisms may influence formation of atherosclerosis and the development of CI. This study was aimed to detect two commonly reported Asp299Gly and Thr399Ile polymorphisms in TLR4 gene in Hunan Han Chinese and their possible relationship with CI. By using the method of polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), the polymorphisms TLR4, Asp299Gly and Thr399Ile, were determined in 366 CI patients and 200 controls from Changsha area of Hunan Province. Carotid intima-media thickness (CIMT) also was detected by Bmode ultrasonography. Our results suggested both the TLR4, Asp299Gly and Thr399Ile, genetic polymorphisms were not observed in all subjects from Hunan Changsha. Therefore, we speculate they might not be an important factor in the development of CI in the Chinese. [ABSTRACT FROM AUTHOR]

Background: The atherogenic index of plasma (AIP) is an important alternative metabolic biomarker of atherosclerosis and cardiovascular diseases. Nevertheless, the correlation between the AIP and carotid atherosclerosis is unknown among the general population. Methods: A total of 52,380 community residents, aged ≥ 40 years who underwentcervical vascular ultrasound from December 2017 to December 2020 in Hunan China, were selected for retrospective analysis. The AIP was calculated as a logarithmically converted ratio of triglycerides (TG) to high-density lipoprotein-cholesterol (HDL-C). The participants were divided into AIP quartile groups (Q1-Q4). Logistic regression models and restricted cubic spline analyses were used to examine the association of the AIP with carotid atherosclerosis. Stratified analyses were applied to control for confounding factors. The incremental predictive value of the AIP was further assessed. Results: After adjusting for traditional risk factors, an increased AIP was associated with a higher rate of carotid atherosclerosis (CA), increased carotid intima-media thickness (CIMT), and plaques [odds ratio, OR (95% confidence interval, CI): 1.06 (1.04, 1.08), 1.07 (1.05, 1.09), and 1.04 (1.02, 1.06) per 1-SD increase in the AIP, respectively]. Compared with those participants in the quartile 1 group, those in the quartile 4 group had a greater risk of CA [OR 1.18, 95% CI (1.12, 1.25)], increased CIMT [OR 1.20, 95% CI (1.13, 1.26)], and plaques [OR 1.13, 95% CI (1.06, 1.19)]. However, we did not observe an association between the AIP and stenosis [0.97 (0.77, 1.23), p for trend = 0.758]. Restricted cubic spline analyses also showed a cumulative increase in the risk of CA, increased CIMT, and plaques but not stenosis severity (> 50%) with an increase of the AIP. Subgroup analyses showed that a more significant association between the AIP and the prevalence of increased CA was detected in younger subjects (aged < 60 years) with a body mass index (BMI) of ≥ 24 and fewer comorbidities. Additionally, the AIP provided incremental predictive capacity over established risk factors for CA, as shown by an improvement in the net reclassification index (NRI) and integrated discrimination index (IDI) (all P < 0.05). Conclusions: An elevated AIP in a community-based population is associated with a higher rate of CA. the AIP could serve as a potential biomarker for CA risk assessment. [ABSTRACT FROM AUTHOR]

Ischemic stroke is a prevalent disease that seriously threatens human health. It is characterized by high morbidity, mortality, disability, and recurrence rates, causing a significant economic burden on individuals and society. Circular RNA, a novel non-coding RNA, not only serves as the sponge for microRNAs and proteins but also promotes transcription of their parental genes and translates into peptides. In recent years, circRNAs have emerged as key regulators in ischemic stroke. This article aims to provide new ideas about the pathogenesis and progression of ischemic stroke by reviewing the roles of circRNAs in cerebral ischemic injury and summarizing the association between circRNAs and risk factors for ischemic stroke. [Display omitted] • The incidence of IS has been increasing consistently, while effective prevention and treatment methods are still lacking. • CircRNA is closely associated with risk factors for IS and plays a vital role in neuronal injury and vascular endothelial injury after IS. • Coronavirus infections have been linked to cerebrovascular diseases. • CircRNAs have potential as biomarkers for the diagnosis of IS. [ABSTRACT FROM AUTHOR]

The online version of the original article can be found at https://doi.org/10.1186/s12933-023-01839-y B Correction to: Cardiovascular Diabetology (2023) 22:125 b https://doi.org/10.1186/s12933-023-01839-y Following publication of the original article [[1]], the author noticed the error in figure. In the image of Figure 1D, the forest plot of Figure 1D does not match the corresponding odds ratio (OR) and 95% confidence interval (CI). [Extracted from the article]

Background and aims microRNA223 (miR-223) plays an important role in the development of atherosclerosis and ischemic stroke. It is involved in regulation of multiple physiological and pathophysiological processes such as cholesterol metabolism, endothelial cell (EC) function, and thrombosis. Here we investigated the role of methylation regulation of MIR-223 promoter region in atherosclerotic cerebral infarction (ACI) patients. Methods A total of 23 patients with ACI and 32 healthy individuals were recruited. We performed bisulfite sequencing PCR and real-time PCR to detect methylation levels of MIR-223 promoter region and miR-223, respectively, in genomic DNA isolated from peripheral blood leukocytes. Results Mean methylation levels of a total of nine CpGs of MIR-223 promoter were significantly lower in ACI patients than in healthy individuals ( p < 0.01), and were also significantly lower in individuals with carotid atherosclerosis than those without carotid atherosclerosis ( p < 0.05). Meanwhile, miR-223 expression in leukocytes was significantly higher in ACI patients than in healthy individuals ( p < 0.05). miR-223 level was negatively correlated with mean methylation levels of MIR-223 promoter ( r = −0.4451, p < 0.01). The methylation level of MIR-223 promoter revealed a positive correlation with the circulating total cholesterol level ( r = 0.318, p = 0.019). Conclusions Hypomethylation of MIR-223 promoter is associated with atherosclerotic cerebral infarction. [ABSTRACT FROM AUTHOR]

The Basigin (BSG, also known as CD147/extracellular matrix metalloproteinase inducer) belongs to the immunoglobulin superfamily (IgSF). It is a cellular receptor for cyclophilin A (CypA), and is originally known as tumor cell collagenase stimulatory factor (TCSF), which could abundantly expressed on the surface of tumor cells, haematopoietic, monocytes, epithelial endothelial cells and smooth muscle cells. Accumulating evidence showed that BSG played an important role in stimulating the secretion of matrix metalloproteinases (MMPs), which has been reported to be involved in the development of atherosclerosis. Since atherosclerosis is an important risk factor for atherosclerotic cerebral infarction (ACI), we speculate that BSG genetic polymorphisms may influence formation of atherosclerosis and then development of ACI. This study aimed to detect the potential association of the single nucleotide polymorphisms (SNP, −631 G > T, −318 G > C, 10141 G > A and 10826 G > A) of BSG gene in Hunan Han Chinese population with ACI. We genotyped 199 ACI patients and 188 matched healthy controls for the four BSG SNP by method of matrix-assisted laser desorption/ionization-time-offlight mass spectrometry (MALDI-TOF MS). Our results suggested that all the polymorphisms were observed in the subjects from Changsha area of Hunan Province. However, no significant difference was observed between the distribution of these SNP in cases and controls. Therefore, we speculate that BSG genetic polymorphisms might not be an important factor in the development of ACI in our Chinese Han population. [ABSTRACT FROM AUTHOR]

Abstract: Endothelial cells (ECs) apoptosis induced by oxidized low-density lipoprotein (ox-LDL) is thought to play a critical role in atherosclerosis. MicroRNAs (miRNAs) are a class of noncoding RNAs that posttranscriptionally regulate the expression of genes involved in diverse cell functions, including differentiation, growth, proliferation, and apoptosis. However, whether miRNAs are associated with ox-LDL induced apoptosis and their effect on ECs is still unknown. Therefore, this study evaluated potential miRNAs and their involvement in ECs apoptosis in response to ox-LDL stimulation. Microarray and qRT-PCR analysis performed on human umbilical vein endothelial cells (HUVECs) exposed to ox-LDL identified 15 differentially expressed (4 up- and 11 down-regulated) miRNAs. Web-based query tools were utilized to predict the target genes of the differentially expressed miRNAs, and the potential target genes were classified into different function categories with the gene ontology (GO) term and KEGG pathway annotation. In particular, bioinformatics analysis suggested that anti-apoptotic protein B-cell CLL/lymphoma 2 (Bcl-2) is a target gene of miR-365, an apoptomir up-regulated by ox-LDL stimulation in HUVECs. We further showed that transfection of miR-365 inhibitor partly restored Bcl-2 expression at both mRNA and protein levels, leading to a reduction of ox-LDL-mediated apoptosis in HUVECs. Taken together, our findings indicate that miRNAs participate in ox-LDL-mediated apoptosis in HUVECs. MiR-365 potentiates ox-LDL-induced ECs apoptosis by regulating the expression of Bcl-2, suggesting potential novel therapeutic targets for atherosclerosis. [Copyright &y& Elsevier]