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
- Asthma remains a significant global health burden characterised by high clinical heterogeneity and immunological complexity. Despite currently available therapies, limitations like steroid insensitivity and adverse side effects persist. Furthermore, recent biologics' high costs and accessibility remain a constraint. This emphasised the need for innovative alternative treatments. Kaempferol, a naturally occurring flavanol found in various fruits, vegetables, and medicinal plants, has gained considerable attention for its multifaceted pharmacological properties. This review critically assesses existing preclinical evidence regarding the therapeutic potential and molecular mechanisms of kaempferol in experimental asthma models. Preclinical in vivo and in vitro studies consistently demonstrate that kaempferol targets three critical dimensions of asthma pathogenesis: airway inflammation, hyperresponsiveness, and airway remodelling. Mechanistically, it suppresses the infiltration of inflammatory cells and reduces the secretion of pro-inflammatory cytokines, chemokines, and IgE. These effects are achieved by modulating key signalling pathways, including NF-κB, MAPKs, JAK/STAT, Nrf2, and NOX4-mediated autophagy. Furthermore, kaempferol alleviates smooth muscle hypercontractility and suppresses airway remodelling by mitigating subepithelial fibrosis, mucus hypersecretion, and epithelial-to-mesenchymal transition. Its translational strengths include potential steroid-sparing effects. Despite this, its clinical application is hindered by poor oral bioavailability and a lack of direct human trials. Rigorous clinical validation and advanced targeted delivery systems are required to establish kaempferol as a viable therapeutic agent for asthma management. - Source: PubMed
Publication date: 2026/09/05
Lee Yu ZhaoVoon Fui-LingChung Hong YeeShakwat JaimahTham Chau LingHo Yu-ChengLee Ming Tatt - Endometriosis (EMs) is one of the most common gynecologic diseases, and the roles of ferroptosis in EMs have not been fully clarified. The induction of ferroptosis has been demonstrated to inhibit the growth of ectopic lesions in EMs. Although acetyl-CoA carboxylase 1 (ACC1), the rate-limiting enzyme for fatty acid biosynthesis, has been shown to regulate ferroptosis, the detailed mechanism involved has not been fully elucidated. In addition, the role of ACC1, encoded by ACACA, in EMs remains unclear. Thus, the present study aimed to explore the role of ACC1 in ferroptosis and the potential therapeutic effect of the ferroptosis inducer the ferroptosis inducer 56 (FIN56) in EMs. - Source: PubMed
Publication date: 2026/06/29
Zeng ChengZhu JingwenLu RuihuiWu PeiliLi XinLi FangyuanPeng ChaoZhou YingfangXue Qing - Ferroptosis has been shown to participate in luteolysis, yet the upstream signals and metabolic remodeling that trigger it remain unknown. This study aims to clarify these mechanisms. - Source: PubMed
Publication date: 2026/09/04
Li FeiSong JiaHaoZou WeiZhang YuluCheng YanMinZhao HongRuYang BeiKuang Haibin - The seven isoforms of the NADPH oxidase (NOX) family-NOX1-5, DUOX1, and DUOX2-are multidomain enzymes that require distinct regulatory subunits for activation. These enzymes are major sources of reactive oxygen species (ROS), particularly the superoxide anion (O2·-), which exerts both cytotoxic and signalling effects. NADPH acts as a critical electron donor, maintaining cellular redox homeostasis and supporting anabolic metabolism. Dysregulated NOX activity has been linked to metabolic reprogramming in cancer and oxidative stress-induced complications in diabetes mellitus. - Source: PubMed
Publication date: 2026/08/27
Aziz NamraWal AnkitaAlvi InshrahTiwari SakshiYadav Ritu RaniSharma AayushKhan AbidaTandey Roshni - Laryngeal squamous cell carcinoma (LSCC) remains a clinically challenging malignancy of the head and neck. Because organ preservation is a major therapeutic objective in LSCC, stromal biology is of particular clinical relevance. Stromal factors influence local disease control, functional outcomes, and treatment resistance. Cancer-associated fibroblasts (CAFs) are dynamic regulators of extracellular matrix remodeling, immune exclusion, angiogenesis, and therapeutic resistance. However, LSCC-specific evidence remains fragmented, and many mechanistic concepts are still extrapolated from head and neck squamous cell carcinoma (HNSCC) and hypopharyngeal squamous cell carcinoma (HPSCC). This review adopts an evidence-stratified framework that distinguishes direct LSCC evidence from translatable cross-site evidence and hypothesis-generating inferences. We propose a provisional five-state model for LSCC that includes myofibroblastic, inflammatory, antigen-presenting, extracellular matrix-remodeling, and putative immune-trapping CAF programs. Direct LSCC studies support the presence of early stromal activation along the leukoplakia-to-carcinoma continuum and the enrichment of -positive and -positive fibroblastic programs in metastatic disease. Associations involving stromal PD-L1 expression and altered CAF-derived exosomal microRNA cargo have also been reported. Translatable evidence from HNSCC implicates TGF-β- and CXCL12-dependent T-cell exclusion together with Gal9-mediated T-cell dysfunction. Additional mechanisms include IL-6/JAK/STAT3-driven myeloid skewing and NOX4-dependent stabilization of the myofibroblastic phenotype. We integrate these findings into a spatially informed conceptual framework encompassing the invasive front, the perivascular compartment, the cartilage interface, and the lymphovascular niche. We also discuss biomarker-guided therapeutic opportunities, including CAF normalization, -directed approaches, stromal signaling blockade, extracellular matrix-targeted strategies, and interference with extracellular vesicle-mediated signaling. This review thereby establishes an evidence-stratified framework for CAF heterogeneity in LSCC and clarifies the translational value and current limitations of stroma-targeted strategies. It further provides a structured foundation for hypothesis-driven clinical and experimental investigation in laryngeal cancer. - Source: PubMed
Publication date: 2026/08/20
Hong Wei-ZheHuang Guan-JiangLuo Qi-PingLu Biao-Qing