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
- Diabetic retinopathy (DR) is a neurodegenerative disease characterized by hyperglycemia-induced inflammation, mitochondrial dysfunction, and progressive neuronal cell death, leading to irreversible vision loss. Retinal ganglion cells (RGCs) are particularly vulnerable to this hostile microenvironment, undergoing apoptosis before microvascular pathology becomes clinically evident. However, therapeutic strategies targeting these early neurodegenerative events remain limited. Here, we investigated the protective effects of the Annexin A1 mimetic peptide Ac using complementary human retinal organoid (RO) and organoid-derived retinal ganglion cell (RGC) models of diabetes-like stress. In retinal organoids, Ac significantly attenuated high glucose-induced retinal degeneration by coordinately suppressing intrinsic and extrinsic apoptotic pathways, reducing Müller cell gliosis, and selectively modulating inflammatory mediators associated with DR progression. In organoid-derived RGCs, Ac reduced mitochondrial oxidative stress, restored mitochondrial bioenergetics, and prevented neuronal apoptosis under both hyperglycemic and inflammatory conditions. Mechanistically, these protective effects were associated with FPR2-dependent suppression of the p38/NOX4 signaling axis, identifying oxidative stress regulation as a central mechanism underlying mitochondrial preservation. Collectively, our findings demonstrate that Ac acts as a pro-resolving neuroprotective agent that targets convergent inflammatory and mitochondrial pathways involved in early diabetic retinal degeneration, highlighting the FPR2-p38-NOX4 axis as a promising therapeutic target for early intervention in diabetic retinopathy. - Source: PubMed
Publication date: 2026/08/22
da Silva Rafael AndréParween ShamaHowell AnnaHayden SydneyRoberson Paul APeji AleyaGil Cristiane DVergara M Natalia - Keloids are a refractory fibroproliferative disorder characterized by excessive extracellular matrix (ECM) deposition and invasive growth beyond the original wound boundaries, severely impairing patients' quality of life. Accumulating evidence highlights that metabolic reprogramming and mitochondrial dysfunction are important in keloid pathogenesis, particularly in regulating the biological behavior of keloid fibroblasts (KFBs). This narrative review focuses on the sustained development and progression of keloids rather than the triggering factors of disease initiation, and systematically reviews the latest research on the interplay between mitochondrial dysfunction and metabolic abnormalities in keloids. Mitochondrial structural and functional impairments directly trigger metabolic reprogramming in KFBs, shifting energy metabolism toward aerobic glycolysis and disrupting lipid and amino acid metabolism. Conversely, metabolic abnormalities exacerbate mitochondrial damage, forming a pathological feedback loop. This reciprocal interaction collectively shapes the pathological features of KFBs: excessive proliferation driven by energy metabolic adaptation, abnormal ECM deposition mediated by pro-fibrotic signaling activation, and persistent chronic inflammation induced by mitochondrial damage-associated molecular patterns (DAMPs) and metabolic byproducts. By clarifying this synergistic mechanism, this review provides insights into novel therapeutic strategies targeting mitochondrial function and metabolic pathways to mitigate keloid progression. Mechanistically, this revision further highlights that HIF-1α, PI3K/Akt/mTOR, AMPK, NOX4, Piezo1/YAP, NLRP3/STING, and lactate-dependent histone lactylation act as signaling hubs that connect mitochondrial injury to glycolysis, lipid remodeling, amino-acid flux, extracellular matrix (ECM) accumulation, apoptosis resistance, and chronic inflammation. - Source: PubMed
Publication date: 2026/08/08
Zhang LianboLi MingxiZhang GuangWang ZichaoQin Haiyan - Temporomandibular osteoarthritis (TMJ OA) is a degenerative disease with pain, abnormal sound, and restricted mouth - opening. Oxidative stress and ferroptosis contribute to its progression, and inflammatory macrophages in the synovium are crucial. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 4 (Nox4), a major Reactive Oxygen Species (ROS) source, is involved in joint disorders, but the mechanism of Nox4 regulating macrophage ferroptosis in TMJ OA is unclear. - Source: PubMed
Publication date: 2026/08/06
Wang YuchengLi QilinZhang WeijiaChao RuiChen XuzhuoWang YexinZhang ShanyongZhen Jinze - Skeletal muscle growth in poultry depends on the proliferation and differentiation of skeletal muscle satellite cells (SMSCs), yet the regulatory landscape governing these processes in quail remains poorly defined. In this study, primary SMSCs were isolated from embryonic day 15 quail pectoral muscle and validated by PAX7 immunostaining and MYHC immunostaining following induction of differentiation. rRNA-depleted RNA-seq was performed at three developmental stages: satellite cells after differential adhesion (DA), proliferating myoblasts (GM), and differentiated myotubes after 4 d (DM4). Transcriptome profiling identified 9,728 common genes expressed in three group, with 1,254 genes differentially expressed across all pairwise comparisons. Functional enrichment analyses indicated a coordinated shift from cell cycle progression in proliferating cells to muscle contraction, oxidative phosphorylation, and calcium signaling during differentiation. Short time-series expression miner (STEM) analysis revealed distinct temporal expression patterns, highlighting proliferation-associated regulators (e.g., KDR, PIK3R1, MYF5, MYF6, NOTCH1, and WNT2) and myotube-related genes (e.g., ALDH18A1, HOXC8, TBX5, and EN1) as central nodes within stage-specific networks. In addition, 935 lncRNAs and 13,588 circRNAs were detected, many displaying stage-specific expression patterns. Predicted lncRNA-mRNA interactions and circRNA host gene enrichment implicated these noncoding RNAs in muscle development and metabolic remodeling. A competing endogenous RNA network highlighted miR-466-x and novel-m0255-5p as potential post-transcriptional regulators of muscle-related genes, including VEGFA, HDAC4, MYLK4, and NOX4. These findings provide a comprehensive transcriptomic resource for quail myogenesis and identify candidate coding and noncoding regulators relevant to muscle growth in poultry. - Source: PubMed
Publication date: 2026/08/03
Liu JingJiang HongxiaXiao XiaoyunLiao ZurongWang YuxiangDing ZhenxvanChai XuewenLiu HaodongHuang XvwenWei WenhuaXie YunongLiu LuoyangWang ZikunHu XiaolongLiu SanfengChen BiaoMao Huirong - - Source: PubMed
Publication date: 2026/08/17
Che HongZhao BingjieYi WenjingLiu PeijiaHu Lian