Human VCAM-1 / CD106 Protein
- Known as:
- Human VCAM-1 / CD106 Protein
- Catalog number:
- VC1-H5224
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Human VCAM-1 / CD106 Protein
Related genes to: Human VCAM-1 / CD106 Protein
- Gene:
- VCAM1 NIH gene
- Name:
- vascular cell adhesion molecule 1
- Previous symbol:
- -
- Synonyms:
- CD106
- Chromosome:
- 1p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-10
- Date modifiied:
- 2016-10-05
Related products to: Human VCAM-1 / CD106 Protein
Related articles to: Human VCAM-1 / CD106 Protein
- This study aimed to evaluate, through a systematic review and meta-analysis of randomized controlled trials (RCTs), the effects of hesperidin and hesperidin-containing citrus interventions on biomarkers of inflammation, oxidative stress, and endothelial function in overweight or obese individuals. Two authors independently searched PubMed, Web of Science, Embase, Scopus, and the Cochrane Library from inception to April 4, 2026. Methodological quality was assessed using the Cochrane Risk of Bias 2 tool (RoB 2), and certainty of evidence was evaluated with the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach. Heterogeneity was assessed using Cochran's test and the -square ( ) statistic, and fixed- or random-effects models were applied as appropriate. Most continuous outcomes were pooled as mean differences (MDs) with 95% confidence intervals (CIs), whereas total antioxidant capacity (TAC) was pooled as standardized mean differences (SMDs; Hedges' ) due to inconsistent assay methods. Sixteen RCTs involving 845 participants were included. Compared with placebo or control, hesperidin-related interventions reduced C-reactive protein/high-sensitivity C-reactive protein (CRP/hsCRP) (MD: -0.43 mg/L, 95% CI: -0.68, -0.17, = 0.001; GRADE = moderate), tumor necrosis factor-alpha (TNF-α) (MD: -2.84 pg/mL, 95% CI: -4.81, -0.86, = 0.005; GRADE = very low), and vascular cell adhesion molecule-1 (VCAM-1) (MD: -27.16 ng/mL, 95% CI: -50.13, -4.19, = 0.020; GRADE = very low), with no significant effects on interleukin-6 (IL-6), TAC, or intercellular adhesion molecule-1 (ICAM-1). Malondialdehyde (MDA) and superoxide dismutase (SOD) were reported narratively in single studies. Current randomized evidence suggests that hesperidin-related interventions are associated with a modest reduction in CRP/hsCRP, representing the most consistent biomarker signal to date. Evidence for TNF-α and VCAM-1 remains very low in certainty, and findings for IL-6, oxidative stress markers, and ICAM-1 remain inconclusive. Marked between-study differences in intervention matrix, design structure, and reporting methods preclude dose- or matrix-specific recommendations at present. Further high-quality randomized trials with longer follow-up, standardized biomarker assessment, and better characterization of formulations are needed. - Source: PubMed
Publication date: 2026/06/26
Zhu KunLi WenLiao TingtingGuo JianlongHuang TingweiChang DeguiYou Yaodong - Although nucleos(t)ide analog (NUC) therapy reduces hepatocellular carcinoma (HCC) incidence in chronic hepatitis B (CHB) patients, HCC can develop despite viral suppression. Identifying predictive biomarkers of HCC during NUC therapy remains clinically important. This study aimed to identify novel biomarkers by proteomic analysis of serum extracellular vesicle (EV) proteins in CHB patients receiving NUC therapy. - Source: PubMed
Publication date: 2026/07/11
Sometani EmiMurai KazuhiroHikita HayatoSung JihyunMuraoka SatoshiToyoda HidenoriTanaka SatoshiMiyake TakayukiKuriki ShinjiFukumoto KenjiShigeno SatoshiMyojin YutaMaesaka KazukiShirai KumikoMakino YukiTahata YukiSaito YoshinobuKodama TakahiroSakamori RyotaroAdachi JunYamada TomomiTakehara Tetsuo - Silver nanoparticles (AgNPs) have emerged as one of the most widely used nanomaterials in medical and consumer products, yet their cardiovascular safety remains inadequately characterized. While their antimicrobial properties are well-documented, accumulating evidence reveals that AgNPs pose a significant threat to the cardiovascular system. Exposure to AgNPs through inhalation, ingestion, or dermal contact enables these particles to enter systemic circulation, where they accumulate in cardiac and vascular tissues in a dose-, time-, and size-dependent manner. Once deposited, AgNPs initiate a cascade of pathological events, including oxidative stress, mitochondrial dysfunction, DNA damage, and disruption of calcium and sodium channel signaling. These molecular disturbances translate into physiological alterations such as bradycardia, atrioventricular conduction block, impaired contractility, and exacerbated ischemia-reperfusion injury. AgNPs also trigger endothelial activation, leading to upregulation of adhesion molecules, namely vascular cell adhesion molecule-1 (VCAM-1), intracellular adhesion molecule-1 (ICAM-1) and recruitment of inflammatory cells, creating a proinflammatory and prothrombotic environment. Elevated cardiac biomarkers, including creatine kinase-MB fraction (CK-MB), brain natriuretic peptide (BNP), lactate dehydrogenase (LDH), and histopathological changes, including pericardial edema, myofibril disorganization, fibrosis, and inflammatory infiltration are consistently observed. Vascular dysfunction manifests as impaired vasorelaxation, enhanced vasoconstriction via endothelin-1 upregulation, thrombosis, and abnormal angiogenesis driven by vascular endothelial growth factor (VEGF) dysregulation. Although plant-based AgNPs have shown cardioprotective potential in limited studies, the overall evidence indicates significant cardiovascular risk. This systematic review synthesizes findings from 38 preclinical studies (35 in vivo, 3 in vitro), providing a comprehensive analysis of AgNP-induced cardiotoxicity with emphasis on oxidative stress, inflammation, and molecular dysregulation as core mechanistic drivers. - Source: PubMed
Publication date: 2026/07/11
Aditya Muhammad RevaHogipranata Michael OwenAdriansyah VitoMuhammad Athaya RahmanardiBaheera Kameela DilisSimanjuntak Artha Maressa TheodoraRahimah Anna FujiKamila Putri AnnisaSulistomo Hikmawan Wahyu - Astrocytic injury and endothelial activation are interconnected processes within the neurovascular system that may contribute to variability in cognitive performance among cognitively unimpaired adults. Glial fibrillary acidic protein (GFAP) reflects astrocytic injury, while vascular cell adhesion molecule-1 (VCAM-1) reflects systemic endothelial activation. We examined whether VCAM-1 modifies associations between GFAP and cognition in cognitively unimpaired Black adults. This cross-sectional analysis included 313 Black adults aged ≥ 45 years enrolled in the Aging Research Characterizing Health Exposome via Social Drivers (ARCHES) study. Cognitive performance was assessed using the Preclinical Alzheimer Cognitive Composite (PACC) as the primary outcome and the Montreal Cognitive Assessment (MoCA) as a secondary outcome. Plasma GFAP and VCAM-1 were quantified using ultrasensitive immunoassays (NULISA™; Alamar Biosciences). Gaussian generalized linear models tested main effects and a VCAM-1 × GFAP interaction, adjusting for age, sex, and years of education; sensitivity analyses additionally adjusted for the Area Deprivation Index (ADI), body mass index (BMI), and apolipoprotein E (APOE) ε4 genotype. VCAM-1 and GFAP did not show independent associations with PACC; however, the VCAM-1 × GFAP interaction was significant (β = -1.36 × 10⁻⁶, 95% CI: -2.43 × 10⁻⁶ to -2.94 × 10⁻⁷, p = 0.013; FDR p = 0.030; standardized β = -0.118) and remained significant after additional adjustment for ADI, BMI, and APOE ε4 status. Associations were not significant for MoCA. These findings suggest that VCAM-1 may modify the relationship between GFAP and cognitive performance in cognitively unimpaired Black adults. - Source: PubMed
Publication date: 2026/07/10
Singh Ramkrishna KBekena SemereWalker Alexis I BZhu YiqiTrani Jean-FrancoisBabulal Ganesh M - Hyperglycemia and elevated saturated free fatty acids are key metabolic stressors implicated in vascular injury. However, the early transcriptional responses of endothelial cells to combined glucose and lipid stress remain incompletely defined. This exploratory in vitro study investigated whether high-glucose conditioning modifies palmitate-associated oxidative and endothelial stress-related gene expression responses in human umbilical vein endothelial cells (HUVECs). - Source: PubMed
Publication date: 2026/07/10
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