Objectives: Endothelial nitric oxide synthase (eNOS) is a type of nitric oxide synthase that mainly exists in the endothelium. It produces nitric oxide (NO) to regulate the function of endothelial cells. Endothelial dysfunction and increased NO metabolites have been shown in animal models of lupus and in lupus patients, so eNOS gene polymorphisms may be important in the pathogenesis of SLE. This study aimed to investigate the association of the single nucleotide polymorphisms (SNPs) of eNOS and paediatric systemic lupus erythematosus (pSLE).
Methods: A total of 91 pSLE cases and 90 healthy controls were used in this study. We divided these patients into 4 subgroups according to kidney or central nervous system involvement. Four selected SNPs in the gene were analysed with MALDI-TOF mass spectrometry. Statistical methods were carried out to investigate the correlation between the SNPs and pSLE.
Results: SNP rs1808593 genotype GT in case group were significantly higher than those in the control group (p=0.047), and the genotype GT had positive correlation with pSLE (OR=1.93, 95% CI: 1.01-3.69). In subgroup C (the patients with central nervous system but no kidney damage), the genotype GT was significantly higher than those in the control group (p=0.028), and the genotype GT was related to pSLE with central nervous system damage (OR=6.24, 95% CI: 1.17-33.15). In male patients, we found SNP rs1808593 genotype GT in pSLE group was significantly higher than in the control group (p=0.0065), and the risk of pSLE increased in patients with genotype GT (OR=8.36, 95% CI: 2.02-34.6).
Conclusions: SNP rs1808593 GT genotype is significantly higher than that in the control group, which may indicate that this genotype increases the risk of pSLE, especially in boys, and also this genotype might increase the risk of central nervous system involvement. Therefore, eNOS gene SNP rs1808593 genotype may have an important role in predicting the occurrence of pSLE and central nervous system complications in pSLE.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Impact of CB1 receptor antagonism on skeletal muscle hypertrophy and metabolic health: a systematic review of preclinical studies.
Hormones (Athens)
January 2025
LABIOEX-Exercise Biology Lab, Department of Health Sciences, UFSC-Federal University of Santa Catarina, Araranguá, SC, Brazil.
The endocannabinoid system (ECS), regulating such processes as energy homeostasis, inflammation, and muscle function, centers around cannabinoid receptors, including CB1. These receptors are mainly located in the central nervous system and skeletal muscles. Hyperactivity of CB1 receptors is linked to metabolic disorders and chronic inflammation, highlighting their potential as therapeutic targets for muscle hypertrophy and metabolic health.
View Article and Find Full Text PDFExploring the role of T cells in Alzheimer's and other neurodegenerative diseases: Emerging therapeutic insights from the T Cells in the Brain symposium.
Alzheimers Dement
January 2025
Center for Motor Neuron Biology and Disease, Columbia University Medical Center, New York, New York, USA.
This proceedings article summarizes the inaugural "T Cells in the Brain" symposium held at Columbia University. Experts gathered to explore the role of T cells in neurodegenerative diseases. Key topics included characterization of antigen-specific immune responses, T cell receptor (TCR) repertoire, microbial etiology in Alzheimer's disease (AD), and microglia-T cell crosstalk, with a focus on how T cells affect neuroinflammation and AD biomarkers like amyloid beta and tau.
View Article and Find Full Text PDFDisrupted Cross-Scale Network Associated With Cognitive-Emotional Disorders in Sudden Sensorineural Hearing Loss.
CNS Neurosci Ther
January 2025
Department of Otolaryngology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
Background: Sudden sensorineural hearing loss (SSNHL) is associated with abnormal changes in the brain's central nervous system. Previous studies on the brain networks of SSNHL have primarily focused on functional connectivity within the brain. However, in addition to functional connectivity, structural connectivity also plays a crucial role in brain networks.
View Article and Find Full Text PDFHeparin-Binding Protein in Cerebrospinal Fluid as a Biomarker for Bacterial Meningitis: A Study of Diagnostic Accuracy.
Ann Neurol
January 2025
Department of Neurology, Amsterdam Neuroscience, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands.
Objective: We aimed to evaluate the diagnostic accuracy of heparin-binding protein (HBP) in cerebrospinal fluid for the diagnosis of bacterial meningitis in patients with a suspected central nervous system infection.
Methods: This prospective multicenter cohort study determined the diagnostic accuracy of HBP in cerebrospinal fluid (CSF) for bacterial meningitis among a cohort of consecutive patients with a suspected central nervous infection. The final clinical diagnosis was considered the reference standard.
Extracellular Vesicles From Bone Marrow-Derived Macrophages Enriched in ARG1 Enhance Microglial Phagocytosis and Haematoma Clearance Following Intracerebral Haemorrhage.
J Extracell Vesicles
January 2025
Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Microglial phagocytosis of haematomas is crucial for neural functional recovery following intracerebral haemorrhage (ICH), a process regulated by various factors from within and outside the central nervous system (CNS). Extracellular vesicles (EVs), significant mediators of intercellular communication, have been demonstrated to play a pivotal role in the pathogenesis and progression of CNS diseases. However, the regulatory role of endogenous EVs on the phagocytic capacity of microglia post-ICH remains elusive.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!