Ask about this productRelated genes to: GPX3 Blocking Peptide
- Gene:
- GPX3 NIH gene
- Name:
- glutathione peroxidase 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 5q33.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-05-03
- Date modifiied:
- 2015-08-28
Related products to: GPX3 Blocking Peptide
Related articles to: GPX3 Blocking Peptide
- : Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most consumed drugs worldwide and the main cause of drug hypersensitivity reactions (HSRs). The most common NSAID-HSR class is cross-hypersensitivity (CR), with patients reacting to NSAIDs from different chemical groups without specific immunological recognition, with NSAID-induced acute urticaria/angioedema (NIUA) being the most frequent clinical phenotype. Although CR-HSRs are triggered by arachidonic acid (AA) alterations following cyclooxygenase (COX)-1 inhibition and cysteinyl-leukotrienes synthesis by 5-lypoxygenase (5-LO), current evidence supports the participation of additional mechanisms. As COX-1 and 5-LO head oxidative pathways, it is conceivable that enzymes participating in antioxidant control are involved in these mechanisms. In addition, as the CR-HSR susceptibility seems to be influenced by genetic factors, the possibility of genetic variants playing a role in such enzymes should not be excluded. In this observational case-control study, we analysed for the first time in NIUA the overall genetic variability in key antioxidant defence enzymes genes, including catalase (), glutathione peroxidase ()- and , and superoxide dismutase (). We selected a set of tagging single nucleotide polymorphisms (tSNPs) in these genes using data from Europeans in the 1000 Genomes Project. Two independent Spanish populations (discovery and replication) of NIUA patients and NSAID-tolerant individuals were included. : Twenty-six tSNPs were genotyped in the discovery population, with three that were significantly associated with NIUA: rs3448 (GPX-1), rs3792798 (GPX-3), and rs10432782 (SOD-1). They were then genotyped in the replication group, with rs3792798 being protective and rs10432782 being associated with an increased NIUA risk. : Our results suggest that a role for antioxidant enzyme polymorphisms in NIUA is required. Nevertheless, further research is needed to replicate our findings in other populations and their meaning at the molecular level and to investigate the role of such variants in other CR-HSR-induced phenotypes. - Source: PubMed
Publication date: 2026/03/24
Jiménez-Sánchez Isabel MJurado-Escobar RaquelTriano-Cornejo JoséSáenz de Santa María RocíoNúñez RafaelAllali-Bouamara ImaneRaya-López VictoriaChacón PedroLaguna José JTorres María JDoña InmaculadaCornejo-García José A - Keratoconus (KC) is a common eye disease characterized by progressive corneal thinning and steepening. Despite multiple treatment options, there is no definitive cure for KC. Previously we identified loss and dysregulation of nuclear factor erythroid 2-related factor 2 (NRF2) mediated antioxidant functions in stromal cells and extracellular matrix (ECM) in KC. Here we used tear fluid samples and cell culture models to investigate oxidative stress in KC. - Source: PubMed
Koduri Madhuri ACharter MackenzieSonar RohiniDeshmukh RashmiPrescott Christina RMandel RoseSperber LaurenceLee Ting-FangKahan Elias HHaberman Ilyse DSingh VivekBlitzer Andrea LMaiti GeorgeChakravarti Shukti - Renal cell carcinoma (RCC) is the most common type of kidney cancer in adults, with a poor prognosis in advanced stages. Although histological tumor grading is an established prognostic parameter, it often fails to capture the biological heterogeneity of RCC. Therefore, identifying novel biomarkers could enhance early diagnosis and improve predictive accuracy. Here, we aimed to test whether immunophenotypes of specific glutathione peroxidase (GPX) family members may have prognostic value in RCC. - Source: PubMed
Publication date: 2026/04/22
Vageli Dimitra PDoukas Panagiotis GPapageorgiou NikolaosMarkou Chrysanthi AZacharouli KonstantinaIoannou Maria - Implant-related osteomyelitis presents a significant clinical challenge, characterized by bacterial invasion, aggressive inflammation, and impaired osteogenesis. Zn-based implants are biodegradable and bacteriostatic, showing great potential for bone repair, however, the excessive release of Zn ions induces cytotoxicity and impacts early bone formation. To overcome this limitation, biomimetic selenium-doped Ca(PO)SiO nanoleaves (Se-CPS) were fabricated on Zn-1Ca (ZN) substrate. Se-CPS not only moderates the degradation of ZN, maintaining Zn release within a biocompatible range, but also sustainably supplies therapeutic ions (Se, Ca, Si, P) and establishes an alkaline microenvironment. When bacteria invade, the combined action of Zn ions and alkalinity eliminates 75-88% of bacteria by generating abundant intracellular reactive oxygen species (ROS), and concurrently, macrophages clear residual bacteria through enhanced xenophagy, a process driven by regulating the key autophagy-related genes (LC3-I/LC3-II, p62, Beclin 1, FLT4 and ATG5). Following bacterial eradication, antioxidative function of Se-CPS-mediated by the upregulation of selenoprotein genes (GPx1, GPx3, GPx4, TrxR1, SEPSH1, DIO1) restores cell viability and promotes the polarization of macrophages from the pro-inflammatory M1 to the pro-healing M2 phenotype. The combined antibacterial, immunomodulating, and osteogenic effects of Se-CPS were further validated in an osteomyelitis model, demonstrating enhanced osteointegration. This work presents an effective surface engineering strategy for Zn-based implants, enabling simultaneous infection control, inflammation modulation, and accelerated biointegration in an osteomyelitis microenvironment. - Source: PubMed
Publication date: 2026/04/23
Mao MengtingChen JunZhao LinLi QinyanLiu XinyueLiu YanZhang Lan - Psoriasis vulgaris (PV), a chronic immune-mediated inflammatory dermatosis, is associated with a significant burden of systemic comorbidities. Traditional comorbidity research methods struggle to reveal its complex interconnectedness. Based on large-scale retrospective cohort data, we constructed a PV comorbidity network using the Ising model from statistical physics. Weighted network centrality analysis was used to identify core and hub nodes and elucidate shared molecular mechanisms at the multiomics level (nontargeted proteomics and lipid peroxidation metabolomics). Finally, the impact of IL-17A inhibition (IL-17Ai) on PV and atherosclerosis (assessed by carotid Doppler color ultrasound) was evaluated using a prospective intervention study. The Ising model identified atherosclerosis- coronary heart disease (CHD) as the core comorbidity (degree centrality >10), with pulmonary nodules, hypertension, and fatty liver serving as key hub nodes (betweenness centrality >60). Multiomics analysis revealed a core molecular mechanism in PV, involving immune inflammation, oxidative stress, lipid metabolism disorder, and coagulation abnormalities, where the oxidative stress molecule GPX3 acts as a critical hub. Following IL-17Ai intervention, both skin lesions and early atherosclerosis markers significantly improved, accompanied by downregulation of the proinflammatory peripheral blood factor S100A9 and upregulation of anti-inflammatory lipid peroxidation metabolites (e.g., 17(R)-RVD1). This study systematically revealed the modular hierarchical structure of PV comorbidities at the network topology and molecular mechanism levels, confirming the central role of the IL-17 signaling pathway in driving the comorbidity network. This conclusion was further clinically validated by IL-17Ai intervention outcomes. This research provides theoretical and clinical evidence for early identification, prioritized management, and "one drug, multiple targets" therapeutic strategies for treating PV comorbidities. - Source: PubMed
Publication date: 2026/04/14
Shi DongwenLuo YuanZhang PingLiang BinWang MengmengCai HongPang Xiaowen