GPX4 (Isoform a and c)
- Known as:
- GPX4 (Isoform a c)
- Catalog number:
- Y213575
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- GPX4 (Isoform and )
Related genes to: GPX4 (Isoform a and c)
- Gene:
- GPX4 NIH gene
- Name:
- glutathione peroxidase 4
- Previous symbol:
- -
- Synonyms:
- PHGPx, MCSP
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-05-03
- Date modifiied:
- 2014-11-19
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- Acute extremity compartment syndrome (AECS) is a severe surgical emergency with no effective non-invasive therapies available. Here, we demonstrate that low-intensity pulsed ultrasound (LIPUS) attenuates muscle damage by suppressing oxidative stress and ferroptosis. In skeletal muscle cells following hypoxia-reoxygenation (H/R), LIPUS reduced reactive oxygen species (ROS), malondialdehyde, lipid peroxides, and ferrous iron accumulation. In a rat AECS model, LIPUS (1 MHz, 0.5 W/cm, 20% duty cycle) mitigated histopathological injury and iron deposition compared with untreated controls, without affecting healthy muscle. Mechanistically, LIPUS activated the Nrf2/Gpx4 antioxidant pathway and downregulated p53 expression. These findings identify LIPUS as a non-invasive intervention that inhibits ferroptosis and improves tissue outcomes in AECS, suggesting its potential as a bedside therapeutic strategy to complement surgical management. - Source: PubMed
Publication date: 2026/03/21
Ren XiaoboHu YaxinLiu DonghuaWang GuihuaZhai PengLi ZhenzhouSun LeiChen XinLu Minhua - To investigate the associations between urinary and serum metal levels and neurodegenerative diseases (NGDs) as well as all-cause mortality, and identify research trends through bibliometric. - Source: PubMed
Publication date: 2026/04/01
Zhang PeiyunJin WeiLyu XinxuanZhu ShuaiboLu YanbingChen YuzhenHan LuTao MingLi Lihong - Cerebral ischemia-reperfusion injury (CIRI) remains a major cause of neurological disability and lacks effective neuroprotective interventions. Soy isoflavones (SI), phytoestrogens with antioxidant and anti-inflammatory properties, have shown neuroprotective potential. Given that ferroptosis contributes to CIRI pathogenesis and AMP-activated protein kinase (AMPK) regulates redox homeostasis, iron metabolism, and lipid peroxidation, we investigated whether SI protect against CIRI by activating AMPK and inhibiting ferroptosis. - Source: PubMed
Publication date: 2026/04/02
Wu CailianLuo TiantianHuang JinfengMo Ruikang - Diabetes mellitus is a chronic metabolic disorder in which endothelial dysfunction plays a pivotal role in disease progression. (PSP) exhibit multiple biological activities, including antioxidant effects, anti-apoptotic action, and regulation of lipid metabolism. However, the mechanisms by which PSP protects against diabetic endothelial injury remain poorly understood. Therefore, this study aimed to elucidate the protective role and underlying mechanisms of PSP in diabetes-induced vascular endothelial injury. In this study, PSP treatment markedly alleviated diabetes-induced vascular endothelial injury, reduced serum TG and LDL levels in streptozotocin (STZ)-induced diabetic rats. Proteomic enrichment analysis revealed that PSP modulates multiple molecular pathways related to oxidative stress, lipid metabolism, and apoptosis. Further experiments showed that PSP treatment restored mitochondrial membrane potential, enhanced cell viability, suppressed Caspase-3 and Bax expression, and upregulated Bcl-2 to attenuate palmitic acid (PA)-induced apoptosis in endothelial cells. Moreover, PSP reduced lipid peroxidation products (ROS and MDA) and upregulated the expression of Nrf2 and GPX4. In conclusion, PSP effectively alleviates diabetes-induced vascular endothelial injury by improving lipid metabolism, inhibiting apoptosis and oxidative stress, partly through activation of the Nrf2/GPX4 pathway. These findings highlight the potential of PSP as a therapeutic agent for diabetes. - Source: PubMed
Publication date: 2026/04/07
Wu DongdongZhao JingYang QifanFang RourouXu Shouzhu - Ferroptosis has emerged over the past decade as a compelling therapeutic avenue for cancer, prompting intense interest in strategies that selectively induce or inhibit this form of cell death. Although substantial progress has been made in identifying genes that regulate ferroptosis sensitivity and in developing small-molecule modulators, it remains unclear which molecular targets offer the greatest therapeutic potential in specific tissues and contexts. Here, we highlight fundamental differences between and ferroptosis modulation, with emphasis on the integration of different techniques, mouse models, and how the tumor microenvironment shapes two major ferroptosis surveillance pathways: glutathione peroxidase 4 and ferroptosis suppressor protein 1. We propose that integrating biological constraints and microenvironmental complexity is essential for the rational design and successful translation of ferroptosis-targeted therapies. - Source: PubMed
Publication date: 2026/03/12
Vaughan Alec JPalma MarioUbellacker Jessalyn MPapagiannakopoulos Thales