FTH1 Antibody
- Known as:
- FTH1 Antibody
- Catalog number:
- XW-7700
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- FTH1 Antibody
Related genes to: FTH1 Antibody
- 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 Antibody
Related articles to: FTH1 Antibody
- Well-regulated trophoblast proliferation, migration, invasion, and cell turnover are essential for normal placental development in humans and rodents. Given the established role of oxidative stress in placentation and the redox activity of iron, we investigated whether ferroptosis-associated redox signaling contributes to trophoblast function and placental development. Placental iron profiling revealed significantly elevated total and ferrous iron levels in first-trimester human villi compared with term placentas, accompanied by the transcript levels of several iron uptake- and reduction-related genes, including TFRC, DMT1, ZIP8, STEAP3, and STEAP4, which were elevated in first-trimester villi. Murine placentas also exhibited gestational changes in iron abundance and iron-homeostasis-related gene expression. HO-1 protein abundance was highest during early gestation and declined thereafter, suggesting a potential association between heme degradation and gestational iron homeostasis. In contrast, placental labile iron pool (LIP) levels showed only modest, statistically nonsignificant changes across gestation, suggesting a relatively stable redox-active iron pool. Immunofluorescence analyses demonstrated spatially distinct expression of ferroptosis-associated regulators, with ACSL4 enriched in invasive trophoblast populations and GPX4 predominantly localized in surrounding decidual tissues, suggesting regional heterogeneity in ferroptosis-associated molecular features during placentation. Functional studies in HTR-8/SVneo trophoblast cells further demonstrated that mild ferroptosis-associated redox perturbation induced by low-dose erastin or ferrous iron enhanced trophoblast migration and invasion without overt cytotoxicity. These effects were attenuated by ferrostatin-1, deferoxamine mesylate (DFOM), or the mitochondria-targeted antioxidant MitoQ and were blunted following FTH1 and TFRC knockdown, indicating that trophoblast responsiveness depends on iron availability and ferroptosis-associated redox signaling. Importantly, these pro-invasive effects were preserved under physiologically relevant hypoxic conditions. Together, our findings support a model in which gestational changes in placental iron homeostasis are associated with ferroptosis-related molecular features, while experimentally induced iron-dependent redox signaling modulates trophoblast behavior. Rather than inducing overt ferroptotic cell death, sublethal iron-dependent redox perturbation may act as a signaling mechanism influencing trophoblast function during placental development. - Source: PubMed
Jiang WenxinYang YikeYuan XiaoDeng WeiKilby Mark DBaker Philip NTong ChaoYang Yi - Breast cancer remains a significant clinical challenge, particularly in triple‑negative breast cancer (TNBC), in which therapeutic resistance limits treatment efficacy. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has emerged as a promising strategy to overcome resistance in breast cancer. Among the principal nodulators of ferroptosis, NRF2 functions as a central antioxidant transcription factor that suppresses ferroptotic death by promoting glutathione metabolism and cystine uptake via SLC7A11/system Xc-, while also supporting GPX4-dependent lipid peroxide detoxification and iron-sequestering defenses such as FTH1/FTL. In breast cancer, aberrant NRF2 activation supports tumor progression, survival, stemness, immune evasion, and resistance to chemotherapy, radiotherapy, and targeted therapies. This review summarizes the molecular mechanisms by which NRF2 regulates ferroptosis, including KEAP1-NRF2 signaling, metabolic rewiring, iron homeostasis, lipid remodeling, and crosstalk with p53 and other stress-response pathways. We also highlight key regulators such as PRMT5, NUP62, NR5A2/NCOA3, miR-141-3p, DHODH, and ACSL4/ALOX enzymes that shape ferroptosis sensitivity. Furthermore, the review discusses emerging therapeutic approaches aimed at restoring ferroptotic vulnerability, including direct NRF2 inhibitors, natural products, metal-based compounds, repurposed drugs, and nanotechnology-enabled delivery systems. TNBC is specifically reliant on NRF2-driven antioxidant defenses to maintain redox homeostasis and resist ferroptotic stress, supporting its prioritization as a target population for NRF2-ferroptosis-based therapeutic methods. Collectively, targeting the NRF2-ferroptosis axis offers a compelling avenue for improving breast cancer treatment, especially in resistant and aggressive subtypes such as TNBC. - Source: PubMed
Publication date: 2026/09/27
Mohammad Suleiman IbrahimVasudevan AsokanRodrigues Samreet RaizalTurakulov RustamR Baig MirzaNematov OzodbekTailor Navin KumarSinghal DivyaNayak Priya Priyadarshini - Controlling nanoparticle surface chemistry through synthesis conditions-rather than postsynthetic modification-represents an attractive strategy for tailoring therapeutic behavior. Here, we report that the choice of alkali source during one-pot co-precipitation of polydopamine-coated iron oxide magnetic nanoparticles (PDA-FeO MNPs) determine their physicochemical identity and downstream biological activity. The type of base influenced particle properties: NaOH (MNP1) produced smaller (9.4 nm), well-crystallized particles with a negative PDA shell ( = -25.0 mV), whereas ammonia (MNP2) yielded larger particles (11.2 nm) with a higher positive surface ( = +45.5 mV) charge, which was associated with greater cellular uptake. In HUVEC and SH-SY5Y cells, MNPs were biocompatible at low concentrations. In SH-SY5Y cells, when MNP1 was applied with magnetic hyperthermia (MHT+), ROS levels increased to 38.6%, while the lipid peroxidation MFI red/green ratio decreased from ~65 to ~58, indicating a marked ferroptosis tendency. Conversely, MNP2 caused greater membrane damage, with lower ROS production under MHT+ (12.4%) compare to MNP1 (38.6%) and a smaller decline in the lipid peroxidation ratio (from ~60 under MHT- to ~55 under MHT+) in SH-SY5Y. Notably, MNP2's own ROS levels decreased from MHT- (22.8%) to MHT+ (12.4%), the opposite trend observed for MNP1. Ferroptosis-related cell death was not observed in HUVECs, as assessed by ROS and lipid peroxidation assays. Furthermore, the 5.2-fold increase in gene expression in SH-SY5Y cells following MNP1 treatment suggests that the cells activate intracellular iron buffering as a bioinorganic defense mechanism and that different cell death pathways associated with ferroptosis may be triggered depending on the type of nanoparticle. Critically, the formulation induced neither significant cytotoxicity nor markers of ferroptosis in HUVECs, suggesting a degree of cancer-cell selectivity for MNPs. These findings establish that base-dependent surface engineering of PDA-FeO MNPs yield functionally distinct nanoplatforms and provide a rational foundation for the design of ferroptosis-enhanced magnetothermal cancer therapies. - Source: PubMed
Publication date: 2026/09/26
Solak KübraUnver YagmurMavi Ahmet - Diabetic cardiomyopathy (DCM) is a serious cardiovascular complication specific to diabetes mellitus, with rising global prevalence. Ferroptosis, an iron-dependent form of regulated cell death driven by lethal lipid peroxidation, has been implicated in the pathogenesis of DCM. However, the key regulatory genes remain poorly characterized. This study aimed to identify and validate ferroptosis-related signature genes in DCM. Three murine transcriptomic datasets (GSE123975, GSE155377, and GSE210611) were retrieved from GEO and merged after batch correction. Differentially expressed genes were intersected with weighted gene co-expression network analysis disease-associated module genes and FerrDb ferroptosis annotations to define the ferroptosis-related differentially expressed gene candidate pool. LASSO regression and random forest selection then prioritized hub genes, defined operationally as candidates consistently prioritized by both machine-learning algorithms rather than by network-topological centrality. Classification performance was evaluated by ROC analysis and validated in two independent cohorts (GSE161931 and GSE274500). mMCPcounter estimated immune and stromal infiltration. ScRNA-seq (GSE290095) and spatial transcriptomic (GSE290094) profiling characterized cellular distribution, predicted cardiomyocyte network perturbations and tissue-level expression patterns. High-fat diet/streptozotocin (HFD/STZ)-induced DCM rat models provided experimental validation. and were identified as hub genes, with strong discriminatory performance in the discovery cohort (AUC = 1.000 and 0.988; in-sample estimates, = 26) and independent external validation (AUC = 0.951 and 0.988). Immune profiling linked both genes inversely with vessel scores, and was also linked with eosinophils. Single-cell analysis localized enrichment to cardiomyocytes and endothelial cells, while was broadly expressed across multiple cell types, with elevated levels in DCM. In silico knockout analysis predicted distinct cardiomyocyte network perturbation profiles for and , and spatial transcriptomics revealed modest but disease-specific spatial associations between hub gene expression and ferroptosis driver scores (: rho = 0.123; : rho = 0.154). Both genes were significantly upregulated at mRNA and protein levels in HFD/STZ-induced DCM rats, with concurrent GPX4 depletion, ACSL4 accumulation, and FTH1 reduction consistent with ferroptosis activation. This study identifies and as ferroptosis-related molecular signatures in DCM and provides multistep prioritization and validation spanning bulk transcriptomics, single-cell and spatial transcriptomics, and in vivo experimental verification, offering potential targets for ferroptosis-targeted therapeutic intervention. - Source: PubMed
Publication date: 2026/09/09
Zhou FengZhou Jia-BinZhang LingYan Yi-QingWu DanWei Tian-PengZhang Zhen-YeLiu Huan-HuanShen Jun-XianLiu YingQian Ling-LingWang Ru-Xing - Calcific aortic valve disease (CAVD) is a progressive disorder characterized by valvular calcification and currently lacks effective pharmacological therapies. Sirtuin 1 (Sirt1) has emerged as a cardioprotective factor; however, its role in CAVD remains unclear. The present study aimed to investigate whether Sirt1 attenuates CAVD by regulating iron homeostasis, ferroptosis and mitochondrial function through the nuclear factor erythroid 2‑related factor 2 (Nrf2)/heme oxygenase‑1 (HO‑1)/ferritin heavy chain 1 (FTH1) signaling axis. Sirt1 expression was evaluated in human calcified and non‑calcified aortic valves. Primary human aortic valve interstitial cells (hAVICs) were transfected with pcDNA3.1‑Sirt1 and subjected to osteogenic induction with or without the Nrf2 inhibitor, ML385, or the ferroptosis inducer, erastin. Osteogenic differentiation, mitochondrial function, ferroptosis and Nrf2/HO‑1/FTH1 signaling were analyzed. , apolipoprotein E‑deficient (Apoe‑/‑) mice fed a Western diet containing 21% fat and 0.15% cholesterol (w/w) were treated with the Sirt1 agonist, SRT2104, with or without AAV‑mediated HO‑1 or FTH1 silencing, to evaluate aortic valve calcification. The results revealed that Sirt1 expression was significantly reduced in calcified human valves and osteogenically induced hAVICs. Sirt1 overexpression inhibited osteogenic differentiation, reduced RUNX2 nuclear translocation, restored mitochondrial function and suppressed ferroptosis. Mechanistically, Sirt1 activated Nrf2/HO‑1 signaling, upregulated the downstream effector, FTH1, reduced intracellular Fe2+ accumulation and maintained iron homeostasis. These protective effects were abolished by treatment with ML385 or erastin. In Apoe‑/‑ mice, SRT2104 attenuated aortic valve calcification and pathological remodeling, whereas HO‑1 or FTH1 silencing partially reversed these benefits. Collectively, the present study demonstrates that Sirt1 protects against CAVD by activating the Nrf2/HO‑1 pathway, leading to the FTH1‑dependent maintenance of iron homeostasis, the suppression of ferroptosis, the preservation of mitochondrial function and the inhibition of osteogenic differentiation. These findings identify the Sirt1/Nrf2/HO‑1/FTH1 axis as a potential therapeutic target for CAVD. - Source: PubMed
Publication date: 2026/09/25
Yan FeiShi LeiWang YuechanZhao YingWu YuanyuanXian DubiaoLiang YunhengWang NingCui HongwangZhang Minni