Roles of Single Nucleotide Polymorphisms in the SLC6A2 Gene in the Risk of Vasovagal Syncope Among Children in Eastern China: A Case-Control StudyWang, Li, Zhao
et alHealth Sci Rep (2025) 8 (3), e70585
Abstract: Vasovagal syncope (VVS) is a primary reason for fainting in children, affected by numerous genetic and environmental factors. We designed this study to investigate the impact of SLC6A2 gene polymorphisms and gene-environment interactions on the etiology of VVS in children.This study was conducted with 142 children, comprising 71 VVS patients and 71 healthy controls. Five single nucleotide polymorphisms (SNPs) in the SLC6A2 gene (rs2242446, rs168924, rs2397771, rs5564, and rs5569) were genotyped using TaqMan assays. Clinical and hematological data were analyzed alongside genetic information.The rs2242446 TT genotype was significantly associated with VVS (CC + CT/TT, 31/40 vs. 45/26, χ 2 = 5.55, p = 0.02), and the AA genotype of rs5564 was similarly correlated with increased VVS risk (GG + AG/AA, 39/32 vs. 27/44, χ 2 = 4.08, p = 0.04). No significant associations were identified for rs168924, rs2397771, or rs5569. Additional risk factors include family history, elevated hemoglobin (HB) concentrations, increased mean corpuscular volume (MCV), and low vitamin D levels. Multivariate analysis showed that only rs2242446 remained significantly associated with VVS (CC + CT/TT; OR, 2.54; 95% CI; 1.12-5.75; p = 0.03). Vitamin D deficiency, family history, and certain hematological markers were also notable risk factors.Polymorphisms in the SLC6A2 gene, particularly rs2242446, may increase the risk of VVS in children. Further research is needed to validate these findings and explore therapeutic interventions targeting the norepinephrine system.© 2025 The Author(s). Health Science Reports published by Wiley Periodicals LLC.
Myeloid sirtuin 6 deficiency causes obesity in mice by inducing norepinephrine degradation to limit thermogenic tissue functionWang, Liang, Zhang
et alSci Signal (2025) 18 (877), eadl6441
Abstract: Brown and beige adipocytes dissipate energy to generate heat through uncoupled respiration, and the hormone norepinephrine plays an important role in stimulating brown fat thermogenesis and beige adipocyte development in white adipose depots. Increasing energy expenditure by promoting the function and development of brown and beige fat is a potential approach to treat obesity and diabetes. Here, we investigated the effects of macrophage sirtuin 6 (SIRT6) on the regulation of the norepinephrine content of brown adipose tissue (BAT) and on obesity in mice. Myeloid SIRT6 deficiency impaired the thermogenic function of BAT, thereby decreasing core body temperatures because of reduced norepinephrine concentrations in BAT and subsequently leading to cold sensitivity. In addition, the oxygen consumption rate was reduced, resulting in severe insulin resistance and obesity. Furthermore, macrophage SIRT6 deficiency inhibited BAT thermogenesis after cold exposure or norepinephrine treatment and cold exposure-induced increases in markers of lipid metabolism and thermogenesis in white adipose tissue. Myeloid-specific SIRT6 deficiency promoted H3K9 acetylation in the promoter regions and the expression of genes encoding the norepinephrine-degrading enzyme MAOA and the norepinephrine transporter SLC6A2 in macrophages in BAT, leading to norepinephrine degradation and obesity. Our findings indicate that SIRT6 in macrophages is essential for maintaining norepinephrine concentrations in BAT in mice.
Mechanism of action of aloperine in the treatment of pulmonary arterial hypertension based on network pharmacology and molecular docking methodsWang, Yan, Ma
et alHerz (2025)
Abstract: Pulmonary arterial hypertension is a severe pulmonary vascular disease, marked by high mortality and substantial treatment costs, underscoring the urgent need for the exploration of traditional Chinese medicine as a potential therapeutic strategy for pulmonary hypertension. This study aimed to investigate the underlying mechanisms of aloperine in treating PAH through network pharmacology and molecular docking approaches.The Swiss Target Prediction database was employed to predict molecular targets of aloperine, while Cytoscape was used to construct the "active component-target" network. Disease-associated targets were identified through the GeneCards and OMIM databases and cross-referenced with drug targets to determine effective targets of aloperine for PAH treatment. Analysis of protein-protein interaction (PPI) was conducted using the STRING database. Furthermore, gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were carried out via the Metascape platform.Following screening, 42 molecular targets of aloperine, 1264 disease-related targets, and 23 effective targets of aloperine in treating PAH were identified. The PPI analysis revealed that aloperine targets SLC6A2, ADRA1B, CYP2D6, CCR5, and JAK2, all of which play a therapeutic role in PAH. The GO and KEGG pathway analyses identified relevant biological functions, such as membrane raft organization, G protein-coupled amine receptor activity, and regulation of tube diameter, as well as ten pathways including neuroactive ligand-receptor interaction, the cGMP-PKG signaling pathway, calcium signaling, and vascular smooth muscle contraction. Molecular docking results confirmed the interaction between aloperine and its key targets, with a high docking affinity observed between aloperine and the core target ADRA1A.Network pharmacology analysis demonstrated that aloperine exerts its therapeutic effects in PAH primarily through multi-target and multi-pathway mechanisms, providing a novel direction and foundation for PAH treatment.© 2025. The Author(s), under exclusive licence to Springer Medizin Verlag GmbH, ein Teil von Springer Nature.
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