Ask about this productRelated genes to: ACOX3 Blocking Peptide
- Gene:
- ACOX3 NIH gene
- Name:
- acyl-CoA oxidase 3, pristanoyl
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 4p16.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-17
- Date modifiied:
- 2016-10-05
Related products to: ACOX3 Blocking Peptide
Related articles to: ACOX3 Blocking Peptide
- Peroxisomal metabolism was long regarded as a housekeeping pathway with minimal involvement in cancer. Nonetheless, accumulating data demonstrate that peroxisomal lipid oxidation critically modulates genome stability and antitumor immunity. The acyl-CoA oxidase (ACOX) family-including ACOX1, ACOX2 and ACOX3-catalyzes the initial oxidative step of peroxisomal fatty acid β-oxidation, and governs lipid metabolism, redox homeostasis, as well as acyl-CoA-related post-translational modifications such as lysine crotonylation. Notably, ACOX2 has gained growing attention for its connections with DNA damage sensing, cGAS-STING activation and anticancer immunity. Dysregulated ACOX2 expression correlates with tumor progression, therapeutic response and clinical prognosis across various cancers, though direct functional evidence varies by tumor type. Mechanistically, ACOX2-related lipid metabolism maintains intracellular redox balance and stress adaptation, with its pathway-specific signaling still poorly defined. In clear cell renal cell carcinoma, ACOX2 binds MRE11 to destabilize the MRN complex, inducing cytosolic DNA buildup and cGAS-STING-mediated type I interferon signaling, while its universal role in other malignancies awaits validation. ACOX2 acts in a context-dependent fashion: it exerts tumor-suppressive effects in liver, prostate and lung cancers, yet facilitates metabolic adaptation and chemoresistance under therapeutic stress. This review summarizes ACOX2 as a key integrator of metabolism, immunity and genome integrity, and highlights its translational potential as a cancer biomarker and therapeutic target. - Source: PubMed
Publication date: 2026/05/23
Zheng MeiguiZhao BaihuiChen XiuyingZhao Ying - Dodecamethylcyclohexasiloxane (D6) is a cyclic organosilicon monomer widely used in consumer and industrial products and is increasingly detected in environmental and biological systems. Previous studies have shown that D6 modulates the ecological behavior of the heavy metal cadmium (Cd) in soil and reduces Cd accumulation in plants; however, D6-mediated stress responses to Cd in animals and their underlying mechanisms remain inadequately explored. This study reveals that D6 exerts multi-layered protective effects against Cd toxicity in Caenorhabditis elegans. Cd exposure significantly reduced lifespan, brood size, locomotion, and growth, whereas D6 co-treatment (Cd_D6) improved survival by 20%, increased brood size from 64 ± 4.37-90 ± 1.53 eggs, and partially restored locomotor activity. D6 also reduced germline apoptosis and decreased internal Cd accumulation by more than 30%, while stabilizing Ca homeostasis. Biochemically, D6 reversed Cd-induced declines in glucose, pyruvate, and ATP levels, restored mitochondrial ultrastructure, and lowered ROS and MDA accumulation, alongside partial recovery of antioxidant enzyme activities (SOD, CAT, POD, HK, ATPase). Transcriptomic profiling revealed that D6 counteracted Cd-driven repression of metabolic and mitochondrial pathways, including peroxisomal β-oxidation, ubiquinone biosynthesis, and genes essential for lipid catabolism (e.g., acs-7, acox-3, nkat-1). Weighted gene co-expression network analysis identified a D6-responsive module enriched with regulatory genes associated with metabolic repair and stress resilience. Collectively, these findings identify D6 as a previously unrecognized organosilicon compound that reduces Cd accumulation and reprograms metabolic and mitochondrial functions, thereby improving organismal homeostasis and enhancing resilience to Cd stress. - Source: PubMed
Publication date: 2026/05/18
Shehzad KhurramWan TianyingTu ShuxinWang ZhihengAli WaqarAhsen SaireenBabar SabaZhang Jie - Heat stroke (HS) is the most severe form of hyperthermia, with mortality exceeding 50% in severe cases. The liver is highly vulnerable to HS-induced injury, often triggering multi-organ failure. Although rapid cooling remains the primary treatment, the molecular mechanisms underlying hepatic damage remain elusive, highlighting an urgent need for mechanistic insights, especially given global extreme heat events. We established a HS model by gradually increasing the core temperature of mice from 40°C to 43°C. Mice were sacrificed at each target temperature to collect blood and liver tissues for hematological, biochemical, and histopathological analyses. Transcriptomic profiling was conducted on murine livers, and differentially expressed genes (DEGs) were identified and analyzed. The peroxisome proliferator-activated receptor (PPAR) signaling pathway was identified as a significantly enriched pathway and 12 key DEGs were validated by reverse transcription quantitative PCR (RT-qPCR) to assess temperature-dependent metabolic reprogramming. The expression of CD36, ACOX3, and PPARα was validated by immunohistochemistry at the protein level to investigate their response to heat stress. A graded murine HS model was established and histopathology analysis showed significant liver injury with core temperatures ≥ 42°C, manifesting as weight loss, elevated serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), neutrophilia, thrombocytopenia, hepatocyte necrosis, and sinusoidal congestion. Transcriptomic profiling revealed temperature-dependent DEGs from 41°C onward mainly involved in inflammatory/immune, lipid metabolism, apoptosis, and stress response pathways. DEGs consistently dysregulated across different temperatures were enriched in PPAR, insulin signaling, and endoplasmic reticulum (ER) stress-related pathways. RT-qPCR analysis revealed the altered expression of PPAR-related key genes, indicating functional disruption in lipid metabolism. Immunohistochemistry further confirmed these transcriptomic findings at the protein level, suggesting that heat stress induced reprogramming of the PPAR signaling pathway. Together, these findings suggest that HS-induced liver injury is closely associated with progressive metabolic reprogramming, with dysregulated lipid metabolism playing a central pathogenic role. By combining a murine stepwise HS model and transcriptomic analysis, we identified dysregulated PPAR signaling as a key temperature-dependent feature of liver injury, suggesting its potential role as a temperature-sensing node and therapeutic target. This work provides a framework with precise temporal windows and molecular candidates for the development of mechanism-directed intervention strategies for HS. - Source: PubMed
Publication date: 2026/03/24
Zhu YingLiu WanlinYang ChunyuanMa TengHan MingfeiZhang JinxuZhu YunpingMa Jie - This study emphasizes the potential of folic acid (FA) supplementation in controlling intrauterine growth retardation (IUGR)-induced metabolic problems and improving the long-term health consequences of afflicted individuals. - Source: PubMed
Publication date: 2026/04/08
Zhou LaiyiShen WeiyunLiang CanDong QingyiWang JingweiHe Xiaori - Elucidating the molecular mechanisms underlying beef quality differences is crucial for precision breeding of high-quality cattle. In this study, we first characterized the myofibrillar morphology of high-quality (H group) and low-quality (L group) beef samples using hematoxylin-eosin (HE) staining. Transcriptomic and metabolomic analyses were then conducted to reveal the molecular regulatory basis of quality variation. HE staining revealed highly significant differences in muscle fiber area and diameter between H and L groups ( < 0.01), along with significant differences in muscle fiber density ( < 0.05), but no significant differences in muscle fiber perimeter. Furthermore, by focusing on five core metabolic pathways shared across the transcriptome and metabolome datasets, 30 differentially expressed genes (DEGs) and 14 differentially accumulated metabolites (DAMs) were identified. Pearson correlation analysis revealed synergistic regulation between DEGs and DAMs: modulates umami flavor by regulating inosine accumulation via the purine metabolism pathway; promotes unsaturated fatty acid synthesis and intramuscular fat deposition through carbohydrate metabolism; genes in the glycolysis/gluconeogenesis pathway maintain post-slaughter muscle pH homeostasis, thereby influencing beef tenderness. Collectively, this study integrates morphological and molecular evidence to elucidate the multi-level basis of beef quality formation, providing key candidate genes, metabolites, and pathways for molecular breeding. These findings offer comprehensive theoretical and technical support for the sustainable development of the premium beef industry. - Source: PubMed
Publication date: 2026/02/05
Ma FengyingZhou LeBao YanchunGuo LiliSun JiaxinLi ShuaiZhu LinNa RisuShi CaixiaGu MingjuanZhang Wenguang