Ask about this productRelated genes to: NOX4 antibody
- Gene:
- NOX4 NIH gene
- Name:
- NADPH oxidase 4
- Previous symbol:
- -
- Synonyms:
- KOX-1, KOX
- Chromosome:
- 11q14.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-30
- Date modifiied:
- 2016-10-05
Related products to: NOX4 antibody
Related articles to: NOX4 antibody
- Cystathionine β-synthase (CBS), a hydrogen sulfide (H₂S)-producing enzyme, plays a role in maintaining vascular homeostasis through its dual function of generating H₂S and nitric oxide (NO) within the endothelium. Here, we investigated the role of the CBS/H₂S/NO axis under metabolic stress, using both an in vitro model of lipid overload and an in vivo model of high-fat diet (HFD)-induced obesity. Bovine aortic endothelial cells (BAEC) exposed to sodium palmitate (NaP) exhibited impaired NO signaling, accompanied by increased oxidative stress, as evidenced by elevated reactive oxygen species production and upregulation of Nox4 expression, along with activation of the unfolded protein response, an index of endoplasmic reticulum stress. In parallel, a downregulation of CBS expression and H₂S levels was found. Similarly to NaP, CBS silencing was associated with an impairment in NO signaling, supporting its role in endothelial function. The exogenous source of HS reversed NaP-induced damage in BAEC. Extending these findings in vivo, HFD-fed mice developed metabolic dysfunction in terms of HOMA, insulin resistance, and hyperlipidaemia. This was associated with disrupted NO signaling and increased H₂S levels in the aorta. The rise in HS serves as a protective response to oxidative stress induced by HFD. Collectively, these findings demonstrated a crucial role for endothelial CBS in modulating the interplay between H₂S and NO in metabolic stress associated with obesity. Targeting CBS to enhance both H₂S and NO bioavailability can represent a novel therapeutic approach in obesity-related endothelial dysfunction. - Source: PubMed
Publication date: 2026/05/08
Esposito ErikaIndolfi ChiaraPirozzi ClaudioCorreale MelaniaBello IvanaCasale VeronicaPanza ElisabettaRaso Giuseppina MattaceMeli RosariaSorrentino RaffaellaMitidieri Emmad'Emmanuele di Villa Bianca Roberta - Silica nanoparticles (SiNPs), as common feed additives, are widely applied in livestock diets and pose potential risks to reproductive health owing to their tissue accumulation. In the present study, we explored the effects and underlying mechanisms of SiNPs exposure during in vitro maturation (IVM) of porcine oocytes. The results showed that SiNPs significantly suppress porcine oocyte maturation as evidenced by decreased first polar body (PB1) release rate. Notably, SiNPs significantly induced abnormal expansion of cumulus cells and impaired gap junction intercellular communication (GJIC), accompanied by decreased Connexin 43 (CX43) expression and aberrant F-actin structure. Furthermore, DCFH-DA staining showed that SiNPs significantly increased reactive oxygen species (ROS) levels and malondialdehyde (MDA) content, and decreased the mRNA levels of antioxidant-related genes, including SOD1, SOD2, CAT, GPX1, PRDX2, and NRF2. JC-1 staining showed that SiNPs significantly induced mitochondrial dysfunction via diminished mitochondrial membrane potential (ΔΨm) and aberrant distribution, and decreased the mRNA levels of energy metabolism-related genes, such as NOX4 and COX2. Additionally, SiNPs significantly disrupted lysosomal function and cholesterol trafficking and decreased the mRNA levels of LDLR, NPC1, NPC2, and LAMP2, leading to reduced free cholesterol levels and the mRNA levels of estrogen synthesis-related genes, including STAR, CYP19A1, and HSD-3β. Collectively, SiNPs suppress porcine oocyte maturation, at least partly, through oxidative stress, metabolic disruption, and impaired cholesterol trafficking. - Source: PubMed
Publication date: 2026/05/08
Wang HaoxiangChen FengleiLiu YuanWang ChengfeiLiu QiYang ShengMa ZhiyuYuan Yu-GuoPan Shifeng - Kidney diseases, particularly chronic kidney disease (CKD), represent a significant global health challenge, affecting over 9.5% of the world's population. Both systemic inflammation and oxidative stress are strongly associated with the development of CKD and contribute to the emergence of numerous complications. Renal injury is driven by interconnected molecular pathways that collectively exacerbate inflammation, oxidative stress, and fibrotic responses. The activation of mitogen-activated protein kinase (MAPK)/nuclear factor kappa-B (NF-κB) signaling cascades, along with NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome assembly, synergistically amplifies the inflammatory response. Nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) promotes excessive generation of reactive oxygen species (ROS), whereas impairment of sirtuin 1 (SIRT1)/nuclear factor erythroid 2-related factor 2 (Nrf-2) signaling weakens antioxidant defenses; together, these mechanisms exacerbate oxidative stress. In addition to oxidative stress, hyperglycemia also exacerbates renal damage by activating the transforming growth factor-beta (TGF-β)/hypoxia-inducible factor-1 alpha (HIF-1α) signaling axis, thereby promoting renal fibrosis. Collectively, these events culminate in progressive renal dysfunction. In addition to conventional therapies involving anti-inflammatory and antioxidant agents, emerging studies highlight the therapeutic potential of plant-derived agents in mitigating these pathological disturbances. Luteolin is a naturally occurring flavonoid abundantly distributed in a variety of dietary and medicinal plants, such as parsley, celery, green pepper, and carrots. It is predominantly found in members of the Lamiaceae, Asteraceae, Apiaceae, Fabaceae, and Poaceae families. Several studies highlight luteolin's potential in alleviating renal diseases by targeting key mediators, including NF-κB, NLRP3, MAPK, NOX4, ROS, SIRT1, TGF-β, cytokines, and antioxidants, among others. Thus, considering the broad therapeutic potential of luteolin and the complex pathophysiology of renal diseases, the present study aims to elucidate the mechanisms through which luteolin mitigates renal injury. - Source: PubMed
Publication date: 2026/05/08
Singh LovedeepSingh AnishKattna AyushDalal Diksha - Oxidative stress and inflammation play pivotal roles in the secondary brain injury following intracerebral hemorrhage (ICH). Our previous study on cerebral ischemia showed that TIGAR interacted directly with ATF4, thereby suppressing ATF4-mediated endoplasmic stress. In this study, we investigated whether TIGAR conferred protection against ICH by mitigating oxidative stress and inflammation and the regulatory mechanisms. ICH mouse model was established by microinjection of collagenase VII into the right striatum. Neurological dysfunction score was assessed at 24 h and 72 h post-ICH, and mice were sacrificed and the brains were collected at 72 h post-ICH. We found a significant elevation in TIGAR protein expression in the striatum of ICH mice with increased distribution of TIGAR protein among neurons, microglia and astrocytes. Deletion of TIGAR exacerbated neurological deficits and increased hematoma volume. Conversely, overexpression of TIGAR effectively mitigated neurological deficits, reduced hematoma volume and improved neuronal damage in ICH mice. We demonstrated that TIGAR overexpression significantly attenuated lipid peroxide 4-HNE as well as malondialdehyde content (a lipid oxidation product), while suppressing ROS production. In addition, TIGAR overexpression inhibited NLRP3 inflammasome expression along with caspase-1 cleavage. Moreover, TIGAR overexpression downregulated mRNA levels of inflammatory cytokines IL-1β and IL-6 while impeding microglial transformation into pro-inflammatory M1 phenotype. Intriguingly, TIGAR overexpression exerted inhibitory effects on the expression and activity of ATF4 and NOX4/p22phox involved in intracellular oxidative stress and inflammation regulation. In ICH mice, administration of NOX inhibitor GLX351322 (5 mg·kg·d, i.p. for 2 days) significantly ameliorated the intracerebral hemorrhage injury exacerbated by TIGAR knockdown. Collectively, we demonstrate upregulation of TIGAR proteins with enhanced distribution among neurons and glial cells post-ICH. TIGAR may alleviate oxidative stress and inflammation by inhibiting the ATF4/NOX4/p22phox signaling pathway, thereby reducing ICH-associated neuronal damage. The role and mechanism of TIGAR in intracerebral hemorrhage injury. TIGAR suppresses the ATF4/NOX4/p22phox axis, thereby reducing the production of reactive oxygen species (ROS), which subsequently alleviates oxidative stress and inflammatory responses to mitigate hemorrhagic injury. - Source: PubMed
Publication date: 2026/05/07
Li Yan-YanYuan Jian-RongTang JieChen LeiWu Jun-ChaoQin Zheng-HongSheng Rui - - Source: PubMed
Publication date: 2026/05/05
Guan LinshuMao ZhangYang SenWu GuanlinChen YurongYin LianhongQi YanHan LanXu Lina