FOXO3
- Known as:
- FOXO3
- Catalog number:
- 000062A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- FOXO3
Related genes to: FOXO3
- 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: FOXO3
Related articles to: FOXO3
- Cinnamic acid (CA), a natural phenolic compound with antioxidant and anti-inflammatory properties, has recently attracted attention for its potential protective effects on liver function. This study aimed to evaluate the hepatoprotective effects of CA against carbon tetrachloride (CCl₄)-induced toxicity in mice. - Source: PubMed
Publication date: 2026/09/04
Nomiri SamiraTaebi ReyhanehMohammadi YaserYousefi ToobaAsgari FatemehYazdanimoghaddam FarzanehMortazavi NafisehAmini Abdollah - Age-related fertility decline is an increasingly important challenge in reproductive medicine, driven largely by progressive ovarian aging. The aging ovary undergoes functional deterioration characterized by reduced ovarian reserve and declining oocyte quality, ultimately limiting female reproductive lifespan. Although multiple molecular and cellular processes associated with ovarian aging have been identified, these mechanisms are often discussed independently, limiting an integrated understanding of how they interact within the ovary. In this review, we propose an ovary-centered, multi-mechanistic framework to organize current evidence on ovarian aging and fertility decline. We discuss how genomic instability, telomere attrition, mitochondrial dysfunction, oxidative stress, chronic cellular stress responses, and alterations in ovarian signaling and microenvironmental homeostasis collectively contribute to follicle depletion and impaired oocyte competence. Particular emphasis is placed on signaling pathways involved in follicle activation and stress adaptation, including PI3K/AKT/mTOR, FOXO3, Hippo, and AMPK-Sirtuin networks, while acknowledging that many mechanistic relationships remain incompletely defined in physiological ovarian aging. Building on this integrative perspective, we further evaluate mechanism-oriented intervention strategies, including mitigation of cellular stress, metabolic and signaling modulation, optimization of the ovarian microenvironment, established fertility preservation technologies, and emerging exploratory approaches. By integrating current mechanistic and translational evidence, this review provides a conceptual framework for understanding ovarian aging and highlights future directions for evidence-based fertility preservation and reproductive health management in the context of aging. - Source: PubMed
Publication date: 2026/08/04
Chen JianhuiDuan XiaohuiJing YalingLiu XiaofangZhang YongqiangTang YuqinChen ChuanliangYang JiayanLi XiaohongLin FangZhao Lianfang - Exercise is well-established to alleviate the debilitating age-related muscle decline, while through poorly defined mechanisms, raising concerns about identified exercise mimetics based on the " one target " paradigm. This research seeks to find a novel natural product that mimics the effects of exercise on aging skeletal muscle. Here, using an in silico transcriptome-based screening strategy, we discovered a standard water-soluble tomato concentrate (Wstc) as a top-ranked candidate for improving age-related muscle wasting. We found that Wstc efficiently inhibited muscle atrophy in senescent C2C12 myotubes. Treatment with Wstc in aged mice reduced the activity of aging biomarkers, inflammatory mediators, and oxidative stress in their serum and skeletal muscle. Furthermore, Wstc also protected against age-induced muscle decline by markedly increasing muscle mass and physical performance in aged mice. Mechanistically, Wstc activated the AMPK/FOXO3/Sirt3 axis. Ablation of Sirt3 significantly attenuated the Wstc-mediated suppression of aging-induced muscle atrophy both in vitro and in vivo. - Source: PubMed
Publication date: 2026/08/04
Sun YujieLi TingtingWang YuFan MingcongHuang ZhilianRen YikaiWang KaidiQian HaifengLi YanWang Li - Cisplatin causes nephrotoxicity by accumulating in renal tubular epithelial cells (RTECs). Astragaloside IV (ASIV) shows renoprotective potential, but its mechanisms remain poorly understood. Cisplatin induced nephrotoxicity was established in 8-week-old male C57BL/6 mice via intraperitoneal administration of cisplatin at 20 mg/kg for 48 h. For in vitro studies, HK-2 human proximal tubular epithelial cells were exposed to 50 μM cisplatin for 24 h. Multi-omics approaches were employed to identify novel mechanisms by which ASIV ameliorates cisplatin-induced proximal tubular injury. ASIV markedly reduced serum creatinine and urea nitrogen levels in mice, and ameliorated cisplatin-induced proximal tubular injury both in vivo and in vitro. Moreover, ASIV restored mitochondrial damage, upregulated protein expression of PGC-1α, TOMM20, and PINK1 in RTECs. Mechanistically, RNA-seq and scRNA-seq revealed that cisplatin predominantly affected ADRA1A-mediated mitochondrial biogenesis and mitophagy in proximal tubular cells, accompanied by suppression of the AMPK/FOXO3A pathway. Notably, ASIV upregulated ADRA1A expression, thereby facilitating AMPK and FOXO3A phosphorylation and consequently enhancing mitochondrial biogenesis and mitophagy. Furthermore, dabuzalgron (a selective ADRA1A agonist) recapitulated the protective effects of ASIV. In contrast, the renoprotective action of ASIV against cisplatin-induced proximal tubular injury was largely abrogated by the ADRA1A antagonist tamsulosin in vivo and by ADRA1A-specific siRNA in vitro. These findings identify ASIV as a highly promising renoprotective agent that upregulates ADRA1A expression and activates the AMPK/FOXO3A axis to enhance mitochondrial biogenesis and mitophagy, thereby counteracting cisplatin-induced proximal tubular injury. - Source: PubMed
Wang MengPeng WangWei YaniYu HangxingLuo YanZhang QinGuan XuLi YingWang JianweiLi QiuruiXiong Weijian - Nasopharyngeal carcinoma (NPC) is a multifactorial disease driven by both genetic and environmental factors. The neurogenic locus notch homolog 1 (NOTCH1) gene has dual oncogenic and tumor-suppressive effects that depend on the cellular context. An intronic single nucleotide polymorphism (SNP) in NOTCH1, rs3124599, has been linked to various diseases. However, its involvement in NPC remains unknown. This study aims to explore the regulatory and susceptibility effects of rs3124599 on NPC. - Source: PubMed
Publication date: 2026/08/31
Sultan Mujeeb ARomdhoni Achmad ChusnuWungu Citrawati Dyah KenconoPurwono Priyo Budi