Ask about this productRelated genes to: FTH1 protein
- Gene:
- FTH1 NIH gene
- Name:
- ferritin heavy chain 1
- Previous symbol:
- FTHL6
- Synonyms:
- FTH, PLIF, PIG15, FHC
- Chromosome:
- 11q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: FTH1 protein
Related articles to: FTH1 protein
- Ferroptosis of type II alveolar epithelial (AT2) cells plays a crucial role in the pathological progression of acute lung injury (ALI). Although fibroblast growth factor-2 (FGF2) has been shown to exert protective effects against ALI, the underlying mechanisms remain largely unexplored. - Source: PubMed
Publication date: 2026/04/17
Wang YanZhu PingjunDing YongkaiHan XinjieWang XiWu ShengHuai SiyuanLi NanXu GuogangDu Yingzhen - Ferroptosis is an iron-dependent form of regulated cell death driven by lipid peroxidation and oxidative stress, increasingly implicated in cancer biology. However, its molecular regulation across breast cancer subtypes and its potential systemic manifestations remain incompletely understood. The aim of this study was to identify ferroptosis-associated molecular alterations that are largely shared across subtypes and to evaluate their systemic reflection following localized tissue injury. Tumor and matched normal breast tissues representing major molecular subtypes were analyzed. Global mRNA and miRNA expression profiling was performed using microarrays, followed by validation of selected genes using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). Functional enrichment and protein-protein interaction analyses were conducted to characterize associated pathways. In addition, systemic responses were assessed in patients undergoing fibroadenoma cryoablation through longitudinal blood sampling. Six ferroptosis-related genes (, , , , , ) demonstrated consistent upregulation across all breast cancer subtypes, with higher expression observed in more aggressive tumors. These genes are functionally linked to antioxidant defense, iron metabolism, and oxidative stress regulation, and their coordinated expression pattern is consistent with activation of NRF2-dependent cytoprotective pathways. Downregulation of selected miRNAs may contribute to this expression profile but likely represents a secondary regulatory mechanism. Survival analysis revealed heterogeneous and subtype-dependent associations, with limited and gene-specific prognostic relevance. Cryoablation induced transient increases in circulating levels of the analyzed proteins, reflecting systemic responses to localized tissue injury. In conclusion, breast cancer is characterized by a largely shared ferroptosis-associated molecular signature across subtypes; however, its clinical impact appears to be variable and context-dependent. Systemic detection of related molecular signals suggests potential utility as indicators of tissue stress responses, although their role as specific biomarkers of ferroptosis requires further validation. - Source: PubMed
Publication date: 2026/04/12
Boroń KacperPanfil AgataSirek TomaszSirek AgataZmarzły NikolaWróbel MichalinaWróbel ZbigniewBoron DariuszOssowski PiotrStefaniak MartynaOrdon PawełWyrobiec GrzegorzWyrobiec PiotrKulej WojciechLekston NataliaGrabarek Beniamin Oskar - Exposure to polystyrene nanoplastics (PS-NPs) induces cognitive deficits and hippocampal damage in mice; however, the underlying mechanism remains unclear. The behavioral assessments performed in this study revealed significant impairments in learning and spatial memory in mice exposed to PS-NPs. Mechanistically, PS-NPs triggered oxidative stress in the hippocampus, which activated microglia and drove the excessive formation and release of microglial extracellular traps (MiETs). This sustained neuroinflammatory response, characterized by the release of MiETs and increased levels of proinflammatory cytokines (Tumor Necrosis Factor-α (TNF-α) and Interleukin-1β (IL-1β)), was closely associated with neuronal ferroptosis. Ultimately, PS-NPs induced hippocampal ferroptosis, as evidenced by the loss of mitochondrial cristae, depletion of glutathione (GSH) and glutathione peroxidase 4 (GPX4), elevated lipid peroxidation, and disrupted iron homeostasis, characterized by reduced ferritin heavy chain 1 (FTH1) expression and increased levels of ferrous iron. Notably, the antioxidant N-acetylcysteine (NAC) effectively attenuated oxidative stress, suppressed microglial activation and MiET formation, and reduced neuroinflammation, thereby preventing neuronal ferroptosis and cognitive impairment. Coculture experiments confirmed that PS-NPs-induced MiETs mediate neuronal ferroptosis, and inhibition of ferroptosis ameliorates PS-NPs-driven neuroinflammation. These results demonstrate that PS-NPs induce cognitive impairment primarily through an oxidative stress-driven cascade involving microglial activation, MiET release, neuroinflammation, and hippocampal ferroptosis. - Source: PubMed
Publication date: 2026/05/01
Hu JiaChen YinuoXu LangDai AnqiLi JinquanLiu Xudong - The core pathogenesis of carotid atherosclerosis (CAS) lies in the rupture of vulnerable plaques, with macrophages (MC) playing a critical role in plaque progression and destabilization. However, the functional characteristics of MC subpopulations in CAS remain poorly understood. This study systematically investigates the cellular composition of CAS and the regulatory mechanisms of MC by integrating single-cell RNA sequencing (scRNA-seq), in vitro models, and spatial transcriptomics. Differentially expressed genes upregulated in MC were significantly enriched in multiple signaling pathways, including Lipid and Atherosclerosis, Lysosome, and Antigen Processing and Presentation. Gene Set Variation Analysis (GSVA) revealed higher MC scores for Angiogenesis and Lipid Metabolism in the atherosclerotic core (AC). A total of seven distinct MC subtypes were identified. Pseudotime analysis indicated that IGSF21+ MC constitute the initial cell population, while FABP4+ MC represent the terminal cells along the trajectory. An in vitro atherosclerosis model was established to validate the diagnostic value of SPP1, FTH1, and FTL. Spatial transcriptomics further revealed the spatial connection patterns of the SPP1 signaling pathway network across different cell types. This study provides novel molecular insights into the pathogenesis of CAS and lays the groundwork for developing diagnostic biomarkers and therapeutic targets. - Source: PubMed
Qin RongxingLi CaiqiXu HongyuLai XinyuChen Li - Focal cortical dysplasia (FCD) is a leading cause of drug-resistant epilepsy, whereas its molecular and cellular mechanisms remain poorly understood. This study aimed to characterize the cellular heterogeneity of FCD and investigate the function of ferroptosis in FCD pathogenesis. - Source: PubMed
Zeng QingyangZhu FengjunCao DezhiSun YangLi LinTan ZeshiLi CongRen XiaofanLiu YidiLin ZhiqiangZou Dongfang