FOXO3A Mouse Monoclonal Antibody
- Known as:
- FOXO3A Mouse Monoclonal Antibody
- Catalog number:
- BIN-002309-M11
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- FOXO3A Mouse Monoclonal Antibody
Related genes to: FOXO3A Mouse Monoclonal Antibody
- Gene:
- FOXO3 NIH gene
- Name:
- forkhead box O3
- Previous symbol:
- FKHRL1, FOXO3A
- Synonyms:
- AF6q21, FOXO2
- Chromosome:
- 6q21
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-23
- Date modifiied:
- 2015-08-25
Related products to: FOXO3A Mouse Monoclonal Antibody
Related articles to: FOXO3A Mouse Monoclonal Antibody
- Myocardial ischemia-reperfusion injury (MIRI) remains a critical challenge in the management of acute myocardial infarction due to its complex pathological mechanisms. Ferroptosis, a recently identified form of programmed cell death, is closely implicated in MIRI. Mesenchymal stem cell-derived exosomes (MSC-Exo), characterized by their unique biological properties and low immunogenicity, have emerged as promising therapeutic agents for suppressing ferroptosis. This study investigates the protective role and underlying molecular mechanisms of MSC-Exo in alleviating MIRI by inhibiting ferroptosis through activation of the AMPK/FOXO3 signaling pathway. MSC-Exo were isolated by ultracentrifugation, and their morphology and molecular marker expression were validated using transmission electron microscopy and Western blot analysis. Results showed that PKH26-labeled MSC-Exo were efficiently internalized by AC16 cardiomyocytes, confirming functional interaction with cardiac cells. In a hypoxia/reoxygenation (H/R) model, MSC-Exo pretreatment significantly reduced ferroptosis-associated markers, including reactive oxygen species (ROS), malondialdehyde (MDA), and acyl-CoA synthetase long-chain family member 4 (ACSL4), while upregulating antioxidant factors such as glutathione peroxidase 4 (GPX4) and glutathione (GSH). Experiments with the AMPK inhibitor Compound C further demonstrated that the anti-ferroptotic effects of MSC-Exo are mediated via the AMPK/FOXO3 signaling pathway. In vivo studies using a mouse model MIRI of coronary artery occlusion-reperfusion corroborated the cardioprotective effects of MSC-Exo, as evidenced by improved ST-segment elevation, reduced myocardial fibrosis, and decreased serum levels of cardiac biomarkers CK-MB and cardiac troponin I (cTnI). Collectively, these findings indicate that MSC-Exo exert significant cardioprotection by inhibiting ferroptosis through activation of the AMPK/FOXO3 pathway, offering a novel therapeutic strategy for MIRI management. - Source: PubMed
Publication date: 2026/05/15
Qiu ZixiongHan Bing JieZhang JiankaiCao YifangKuang CiyingCai WeibiaoFu YonglinChen WenjieLiu LuJiang MeiCui Xiaojun - This study aimed to investigate the role of serum- and glucocorticoid-inducible kinase 1 (SGK1) in dry eye disease (DED) pathogenesis and its underlying molecular mechanisms. - Source: PubMed
Tang YunChen ZeyingJiang JiaxuanZhang DiChu YiranLi BodaZhang QiHu Kai - Aging is accompanied by a progressive decline in skeletal muscle mass and function, culminating in sarcopenia, a major contributor to frailty, disability, and mortality in older adults. While skeletal muscle aging has traditionally been attributed to cell-autonomous and local tissue mechanisms, increasing evidence suggests that systemic, cell non-autonomous processes play a central role in coordinating aging across organs. The brain, particularly the hypothalamus, has emerged as a key regulator of organismal aging, yet its contribution to skeletal muscle aging remains poorly defined. Here, we tested the hypothesis that senescence confined to the brain is sufficient to induce aging-like molecular remodeling in skeletal muscle via systemic mechanisms. To model brain senescence, young mice were subjected to fractionated whole-brain irradiation (WBI), a well-established approach that induces widespread cellular senescence and neuroinflammation in the brain while sparing peripheral tissues. Two months after WBI, transcriptomic profiling of quadriceps muscle was performed and compared with that of naturally aged mice. WBI-induced robust gene expression changes in skeletal muscle that closely mirrored those observed during chronological aging. Pathway-level analyses revealed marked downregulation of mitochondrial organization, respiratory chain assembly, and metabolic processes, alongside enrichment of remodeling- and stress-associated pathways. Upstream regulator analysis identified FOXO1, FOXO3, KLF15, and STAT3, which are key drivers of muscle catabolism and atrophy, as central mediators of the observed transcriptional program. Semantic similarity analysis further demonstrated a high concordance between WBI-induced and aging-associated biological processes. Collectively, these findings demonstrate that brain senescence is sufficient to drive sarcopenia-like transcriptomic remodeling in skeletal muscle, implicating central nervous system aging as an upstream regulator of peripheral muscle decline. This brain-muscle aging axis may contribute to frailty in individuals with accelerated brain aging and in cancer survivors exposed to cranial irradiation, highlighting brain senescence as a potential therapeutic target to mitigate systemic aging and skeletal muscle dysfunction. - Source: PubMed
Publication date: 2026/05/14
Ekambaram ShobaPatai RolandGulej RafalKiss TamasChandragiri Siva SaiNagy DorinaKordestan Kiana ValiLakat TamasTarantini StefanoMukli PeterYabluchanskiy AndriyUngvari AnnaBenyó ZoltánCsiszar AnnaUngvari Zoltan - Aging exhibits both systemic and organ-specific components, yet existing models struggle to disentangle their shared versus distinct biological determinants at the population level. We present a structural decomposition framework that partitions seven organ-based biological age gaps (BAGs) into a Common BAG (CBAG) and seven Organ-Specific BAGs (OSBAGs) in 501,388 UK Biobank participants. This dual-axis model outperforms undecomposed body/organ BAG approaches in predicting lifespan, healthspan, and organ-specific disease risk. A large-scale aging GWAS identifies 747 novel loci, complemented by integrative proteomic and metabolomic analyses that reveal causal and druggable targets, including CST1. Pathway-guided multi-omics demonstrates a modular aging architecture, with CBAG reflecting cross-tissue regulators (e.g., FOXO3) and OSBAGs capturing organ-restricted effectors (e.g., UMOD). Drug-aging profiling uncovers organ-specific pro-aging effects consistent with known toxicities that are largely missed by undecomposed models. Sex-stratified analyses further reveal divergent molecular trajectories between males and females. All findings are integrated into HONOR, the first open-access atlas for structural aging and multi-omics translation. - Source: PubMed
Publication date: 2026/05/08
Huang HeLi YiSong QinglinYuan LiyunYang YuqiZhu MinweiSun RenliangHu YueXiong ChenyihangNi TingLiu YunRuiz-Linares AndrésZhang GuoqingLiu FanPeng QianqianWang Sijia - Ferroptosis has recently been implicated in seizure-induced neurodegeneration, whereas enhanced aerobic glycolysis during seizures may aggravate oxidative stress and ferroptotic damage. This study investigated whether inhibition of aerobic glycolysis suppresses ferroptosis through activation of the AMP-activated protein kinase (AMPK)-Forkhead box O3a (FoxO3a) signaling pathway in epileptic rats. - Source: PubMed
Publication date: 2026/05/13
Yang HailinZhong RujieLi XiaoyuWang FeiyuSun LijieTong TongDong HaichengZhai LiGao Jing