Ask about this productRelated genes to: ICAM1 antibody
- Gene:
- ICAM1 NIH gene
- Name:
- intercellular adhesion molecule 1
- Previous symbol:
- -
- Synonyms:
- BB2, CD54
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-04-24
- Date modifiied:
- 2016-01-15
Related products to: ICAM1 antibody
Related articles to: ICAM1 antibody
- Atherosclerosis (AS) remains a leading cause of cardiovascular morbidity and mortality worldwide, with current treatments focused primarily on reducing low-density lipoprotein levels while failing to repair damaged endothelial cells, thus highlighting the urgent need for novel therapeutic drugs. To address this challenge, we analyzed human AS patient single-cell RNA sequencing datasets to identify disease-driving genes and then employed connectivity map analysis to screen for potential therapeutic compounds. Using network pharmacology and machine learning to predict core drug targets, the study validated drug-target interactions through molecular docking, molecular dynamics simulations, and surface plasmon resonance analysis, with experimental validation conducted using endothelial cell damage models and atherosclerotic mice. The integrative approach successfully identified narciclasine as a promising therapeutic compound that targets vascular cell adhesion molecule 1 and intercellular adhesion molecule-1 (VCAM-1/ICAM-1) for AS treatment, with molecular studies confirming strong binding affinity and experimental validation demonstrating significant alleviation of endothelial dysfunction through downregulation of VCAM-1/ICAM-1 expression and reduction of aortic plaque burden in mouse models. This multiplatform methodology combining single-cell sequencing, network pharmacology, machine learning, computational simulation, and experimental validation provides a robust framework for drug discovery while positioning narciclasine as a promising therapeutic candidate warranting clinical investigation for AS treatment. - Source: PubMed
Publication date: 2026/03/27
Wang YangCao ZhenLan HuaiLi BoWang GuixueChen Qingmei - Lungs are highly affected by brain death, with females showing a higher inflammatory response, linked sex hormones acute reduction. With the aging of world population, the number of older donors is increasing. So, the study of menopause associated changes gain importance. Here we investigated menopause's effects in female brain death rats, previously subjected to transitional follicular depletion and aging. Female Wistar rats were divided in young and menopause groups. After follicular depletion, rats aged for 10 weeks. The animals were submitted to brain death and Sham operated rats served as controls. White blood cell counts, bronchoalveolar lavage were analyzed and inflammatory mediators were quantified. Lung tissue was evaluated for myeloperoxidase, intercellular adhesion molecules, miRNA expression, and protein and gene expression of estradiol receptors. In menopause group, there was increase in systemic and tissue leukocyte infiltration, myeloperoxidase expression, inducible nitric oxide synthase, intercellular adhesion molecule-1, lung edema, and loss of IL-10 regulation. Additionally, we found alterations in estradiol receptors along with changes in the expression of miRNAs associated to inflammation, vascular function and senescence. Menopause increases lung inflammation after brain death, by higher leukocyte infiltration and reduction of IL-10 and may impact the outcome of lung transplantation. - Source: PubMed
Publication date: 2026/09/04
Miola Elizabeth CristinaToneto Nicholas Pietro AgulhaYamamoto Ricardo-da-Silva Fernandade Freitas Pedro Luis ZontaVidal-Dos-Santos MarinaMarques Luciana CoelhoLeuvenink Henri Gerrit DerkMoreira Luiz Felipe PinhoCorreia Cristiano JesusBreithaupt-Faloppa Ana Cristina - Polystyrene microplastics (PS-MPs) are environmental pollutants linked to cardiovascular diseases. This study investigated PS-MP-induced vascular toxicity mechanisms in mice. Mice were divided into saline control, low/medium/high PS-MP exposure (0.1, 1, and 10 mg/kg/d), and PS-MPs plus ferroptosis inhibitor Ferrostatin-1 (1 mg/kg/d + Fer-1) for 5 weeks. Vascular histopathology, lipid profiles, oxidative stress, ferroptosis markers, endothelial function, and serum metabolomics were assessed. PS-MP exposure elevated ROS, MDA, TC, and TG while reducing GSH and HDL-C. Ferroptosis was confirmed by decreased GPX4 and SLC7A11, with increased Fe deposition. Vascular endothelial injury and remodeling occurred, evidenced by elevated ET-1, VEGF-A, VCAM-1, and ICAM-1, alongside reduced NO. Metabolomics revealed disruptions in folate, amino acid, citrate cycle, and tryptophan metabolism. Fer-1 inhibited ferroptosis, alleviating endothelial damage and vascular remodeling. PS-MPs induce vascular toxicity through oxidative stress, ferroptosis, and metabolic disturbances, mitigated by Fer-1. - Source: PubMed
Publication date: 2026/09/12
Zhu DeyuLiang XiaoHuang QiWu YangWei ZhuangzhuangCai ShenyangFeng QingMa PingYang XuBao CuiyuBao Xinyu - Bronchopulmonary dysplasia (BPD) affects the most immature preterm infants and can result in long term pulmonary morbidity. Yet, how prenatal and neonatal exposures perturb early proteome maturation and contribute to BPD pathogenesis remains unclear. - Source: PubMed
Publication date: 2026/09/18
Klevebro SusannaPanwar Mohit BWackernagel DirkHansen Pupp IngridBjörkander SophiaDanielsson HannaUhlén MathiasVallin LivSävman KarinPivodic AldinaHellström AnnNilsson Anders K - Xylenes are ubiquitous environmental chemicals associated with central nervous system toxicity; however, their effects on cardiovascular disease are poorly understood. We tested the hypothesis that chronic m-xylene inhalation disrupts vascular homeostasis by inducing endothelial toxicity. Male C57BL/6 J mice were exposed to HEPA-filtered air or m-xylene (50 ppm, 6 h/day, 5 days/week) for 12 weeks. Endothelial injury, platelet activation, immune remodeling, hepatic and pulmonary transcriptomic responses, and plasma metabolomic profiles were assessed using flow cytometry, RNA sequencing, and untargeted metabolomics. The data show that chronic m-xylene inhalation induced a coordinated vascular injury phenotype characterized by 2.4-3.6-fold increases in circulating endothelial extracellular vesicles (EVs), activated endothelial EVs, and endothelial progenitor cell-derived EVs, accompanied by a 60% reduction in circulating endothelial progenitor cells, ~25% increase in soluble ICAM-1, and ~ 50% higher plasma 8-isoprostaglandin F2α levels, indicating endothelial activation, impaired vascular repair, and systemic oxidative stress. m-Xylene exposure also increased platelet-lymphocytes and platelet-granulocyte aggregates by ~25% and platelet-derived EVs by 9-fold, demonstrating thrombo-inflammatory activation. Plasma metabolomics revealed extensive metabolic remodeling, including increased phase II xylene metabolites, bradykinin, cholic acid, and fructose (Log2 fold change >1.5). Transcriptomic analyses demonstrated adaptive hepatic induction of xenobiotic metabolism and antioxidant pathways together with pulmonary inflammatory and immune remodeling. These findings identify endothelial toxicity as an early and sensitive cardiovascular consequence of chronic xylene exposure, provide mechanistic support for epidemiological associations between BTEX exposure and CVD, and identify endothelial EVs, EPC depletion, platelet-derived EVs, and phase II xylene metabolites as promising biomarkers of m-xylene induced vascular injury. - Source: PubMed
Publication date: 2026/09/18
Malovichko Marina VMcFall Samantha ATaylor Breandon SWickramasinghe Nalinie SSithu Israel DConklin Daniel JZelko Igor NSrivastava Sanjay