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
- Preeclampsia (PE) affects 2-8% of pregnancies and causes > 76,000 maternal deaths annually. The mechanistic link between placental oxidative stress and angiogenic failure remains poorly defined, and no validated multi-gene biomarker panel exists for early detection. In particular, how antioxidant enzymes such as PRDX2 interact with angiogenic regulators (VEGFA, ENG) to drive network rewiring in the PE placenta has not been characterized across independent cohorts. This study aimed to characterize the transcriptomic interdependencies between oxidative stress defense, cytokine signaling, and angiogenic regulation across five independent PE placental GEO cohorts. - Source: PubMed
Publication date: 2026/08/10
Kong XiaojuanLiu PengQiao JiangTan ZenyuLei Lei - The NADPH oxidase (NOX) family in humans includes seven enzymes whose main function is to produce reactive oxygen species. Because of their role in oxidative damage, these enzymes are being explored as targets for new therapies against oxidative stress-related diseases. However, their conserved catalytic core poses selective inhibition challenging. Current inhibitors suffer from low potency, cytotoxicity, assay interference, and poor selectivity. VAS2870, a covalent NOX inhibitor targeting a cysteine in the dehydrogenase (DH) domain, does not present assay interference but still shows limited selectivity, solubility, and safety. This study aimed to develop improved VAS2870-based targeted covalent inhibitors (TCIs) by designing and screening a library of cysteine-targeting compounds against NOX1, NOX2, NOX4, and NOX5. A hit compound, compound 2, was optimized, yielding a potent, homolog-selective NOX4 inhibitor, compound 18. Its mechanism of action was validated, demonstrating covalent binding to a cysteine residue and showing that compound binding is hindered by the presence of FAD in the DH domain. - Source: PubMed
Publication date: 2026/08/14
Castelôa MarianaMarchese SaraMassari MartaLima CarlaBasile LorenzoReis JoanaRe MatteoMartins Fábio GSousa Sérgio FLima InêsBenfeito SofiaBorges FernandaMattevi AndreaChavarria Daniel - Aquatic ecosystems are gradually being threatened by intensive agricultural practices, especially the extensive application of pesticides. Although pesticides such as organophosphates, carbamates, pyrethroids, phenylpyrazoles, and neonicotinoids are extensively used in agriculture for pest control, their entry into aquatic environments through runoff, leaching, and atmospheric deposition poses significant risks to nontarget organisms, including fish. This study provides a comprehensive understanding of pesticide-induced toxicity in fish, with particular emphasis on histopathological modifications and genetic alterations in the liver as critical biomarkers of cellular dysfunction, tissue injury, and toxicological responses. At the molecular level, the principal pathways affected included apoptosis (bcl2, caspase 3, 8, and 9), necroptosis (mlkl, ripk1, and ripk3), autophagy (atg and lc3), inflammation (cyp19a, nfκb, tnfα, and nox4), and DNA damage response pathways (atm, atr, tp53, and mdm2) indicating severe cellular stress, genomic instability, and tissue dysfunction induced by pesticide exposure. The major histopathological alterations observed in the liver included vacuolization, hemorrhage, vascular congestion, pyknotic nuclei, and inflammatory cell infiltration. This review highlights an integrated understanding of the association between hepatic histopathological manifestations and molecular responses in fish exposed to pesticides, providing insights into the mechanisms of hepatotoxicity and recognizing possible biomarkers for environmental monitoring and ecotoxicological risk assessment. These biomarkers play a crucial role in assessing the extent of aquatic contamination and understanding the implications of pesticide exposure on fish health, biodiversity, and ecosystem stability. Furthermore, this review underscores the urgent need for effective monitoring and mitigation strategies to safeguard aquatic life and maintain environmental integrity. - Source: PubMed
Publication date: 2026/08/13
Kumar ManojYadav SeemaDubey AasthaJain AnamikaSingh Shefalee - Approximately 10%-30% of elderly patients experience cognitive decline after general anesthesia and surgery. However, how specific brain regions coordinate cellular and molecular networks to mediate cognitive decline remains unknown. Here, we revealed that the hippocampus, but not other cognitive-related brain regions, exhibits increased blood-brain barrier (BBB) permeability, leading to neuroinflammation activation and cognitive decline after general anesthesia and surgery in aged mice. Mechanistically, anesthesia and surgery induce expression of the mechanosensitive channel Piezo1 in hippocampal endothelial cells (ECs) of aged mice. Inducible EC-specific deletion of Piezo1 restores hippocampal BBB integrity, inhibits neuroinflammation activation, and improves cognitive decline in aged mice following anesthesia and surgery. Conversely, injection of the Piezo1 agonist Yoda1 promotes hippocampal BBB breakdown. Moreover, activation of Piezo1 induces Nox4, which mediates hippocampal BBB breakdown and neuroinflammation activation after anesthesia and surgery in aged mice. Therapeutically, AAV-BR1 transduction to brain microvascular ECs for the knockdown of endothelial Nox4 blocks Piezo1-mediated hippocampal BBB breakdown and neuroinflammation activation. Overall, inhibiting the endothelial Piezo1-Nox4 axis restores hippocampal BBB integrity to improve anesthesia- and surgery-induced cognitive decline in aged mice, highlighting potential therapeutic strategies. - Source: PubMed
Publication date: 2026/08/12
Qiu YongMo ChunhengWu JinyanLi JiachenXu ShiyuChen LuZhang LiyinHuang XingmingZhang YiSun MengKang YiZhu TaoDing Bi-SenChen Guo - Decreased apical bicarbonate transport into the airway surface liquid (ASL) has been associated with decreased ASL pH, which can have adverse respiratory effects. However, the human CF epithelium can normalize ASL pH. Thus, we hypothesized that pH regulatory proteins other than the CFTR could be altered in the CF epithelium. - Source: PubMed
Davis Michael DSmith LauraZhao YiRahman Rania AbdulKhalid FaizaChmiel JamesBoyne KatieDaniels Ivana AGaston BenjaminMarozkina Nadzeya