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
- Ferroptosis has been recognized as an important pathological mechanism underlying ischemic stroke (IS). However, the precise mechanisms underlying the neuroprotective effects of Hydroxysafflor yellow A (HSYA) in IS remain unclear. - Source: PubMed
Chen YunChen TianxueYu Li - Heart failure (HF) is the end stage of various cardiovascular diseases, and persistent myocardial injury and adverse remodeling are major causes of its high hospitalization and mortality rates worldwide. Therefore, it is important to identify key molecules and effective agents that can slow or reverse HF progression. Cycloastragenol (CAG) is an active compound derived from Astragalus and has anti-inflammatory, antioxidant, and tissue-protective effects. The present study aimed to clarify the protective role of CAG in HF and to determine whether this effect is related to the regulation of ferroptosis through the PI3K/AKT/mTOR signaling pathway. The results showed that PI3K/AKT/mTOR signaling activity was markedly decreased in myocardial tissue from HF rats, accompanied by impaired cardiac function, aggravated myocardial injury, enhanced inflammatory response, and increased myocardial fibrosis and hypertrophic remodeling. At the same time, GSH levels were decreased, whereas ROS, MDA, and Fe levels were increased. In addition, GPX4 and FTH1 expression was downregulated, ACSL4 expression was upregulated, and the Prussian blue-positive area was increased, indicating marked ferroptosis-related abnormalities. After CAG treatment, these changes were improved to different degrees. CAG restored cardiac function, reduced serum NT-proBNP, CK-MB, and cTnI levels, decreased inflammatory factor expression, and alleviated myocardial fibrosis and hypertrophy. Meanwhile, PI3K/AKT/mTOR signaling activity was restored, and iron deposition, lipid peroxidation, and ferroptosis-related molecular abnormalities were alleviated. In vitro experiments further showed that, in an OGD-induced H9c2 cell injury model, CAG increased cell viability, reduced LDH release, attenuated the inflammatory response, and alleviated mitochondrial membrane potential loss, ROS accumulation, and ferroptosis-related protein abnormalities. C11-BODIPY 581/591 flow cytometry further demonstrated that CAG reduced OGD-induced lipid ROS accumulation and lipid peroxidation. In addition, the ferroptosis inhibitor ferrostatin-1 partially rescued OGD-induced cell injury, restored cell viability, reduced LDH release, and suppressed lipid ROS accumulation, further supporting the involvement of ferroptosis-related processes. Further intervention with the AKT inhibitor MK-2206 partially weakened the protective effects of CAG, supporting the involvement of AKT signaling in its protective action. In conclusion, the present study showed that CAG improved HF-related myocardial injury and myocardial remodeling by restoring PI3K/AKT/mTOR signaling activity and inhibiting ferroptosis-related processes, suggesting that CAG may be a potential therapeutic agent for HF. - Source: PubMed
Publication date: 2026/09/29
Qi ShuboWei DongshengPan PengyuGu WenhaoLiu WenjunZhao ShunJiang YoumingZhang Zhe - Cellular morphological transitions are observed across many diseases, yet their functional role remains unclear because few technologies profile form and function in the same cell. Linking single-cell morphology to transcriptomics is difficult: The two modalities share no feature correspondence and are typically measured in different cells. We present GeoAdvAE, a geometry-aware adversarial autoencoder for diagonal (unpaired) integration of single-cell morphology and single-cell RNA sequencing. GeoAdvAE couples modality-specific variational autoencoders with a Gromov-Wasserstein regularizer and an adversarial discriminator to embed unpaired morphologies and transcriptomes into a shared latent space that preserves both reconstruction fidelity and cross-modal geometry. Using patch-seq neurons with joint morphology-RNA measurements as ground truth, GeoAdvAE attains the best cross-modal cell-type matching accuracy among diagonal integration methods, outperforming optimal-transport, latent-alignment, and adversarial baselines. Applied to 98 CAJAL-quantified microglial morphologies and 31,948 single-cell transcriptomes from the 5xFAD Alzheimer's disease model, GeoAdvAE recovers a one-dimensional axis that aligns the two modalities. Integrated-gradient attribution highlights transcriptomic shifts (DNA repair in ramified microglia; cell killing in amoeboid microglia), nominates gene markers (; /), and reveals disease-associated microglia signatures that are decoupled from morphology. GeoAdvAE provides a scalable, interpretable approach to connecting cellular "form" and "function" when joint profiling of morphology and transcriptomics is impractical. Our method is publicly available at https://github.com/turbodu222/GeoAdVAE. - Source: PubMed
Publication date: 2026/09/29
Du Jinqiu TurboChartrand TomJayadev SumanPrater Katherine ELin Kevin Z - Small extracellular vesicles (sEVs) carry diverse cargo essential for intercellular communication, but their organism-wide characterization across all tissues is still limited. Here, we present a multi-omics sEV atlas covering the whole-body of 120 tissue sites, four body fluids and nine gastrointestinal contents from the same pig. We identified 7995 proteins, 337 miRNAs as well as 105,409 transcripts (93,409 full-length) in sEVs by mass spectrometry, next- and third-generation RNA sequencing. Among these, a conserved cargo set of 252 proteins, 18 miRNAs and 1227 transcripts was defined, including RNA-binding proteins (ANXA2, ALIX and MVP), mitochondrial proteins (ATP5F1A, COX6C and VDACs), the let-7 miRNA family and ferritin genes (FTH1/FTL). Notably, sEV biogenesis-associated ACTG1, CFL1 and ANXA2 were detected in all samples, suggesting their potential as novel sEV protein markers. In contrast, 2638 proteins, 152 miRNAs and 1000 transcripts showed organ-specific expression patterns, which are likely to underpin organ-specific biological processes. Moreover, by using this multi-omic dataset and additional RIP assays, we found that HNRNPU participates in the sorting of hypoxia-responsive EPAS1 into sEVs. This comprehensive sEV atlas establishes a foundation for future studies in sEV cell biology. - Source: PubMed
Yu NaixiangLiu JinxiuLai ChenliangLiu SiyiWei JiachengZhong JiahongXiong SanyaZeng QingjieMa JunwuZhang ZhouZhang Zhiyan - Tubular ferroptosis is increasingly implicated in diabetic kidney disease (DKD), but noninvasive urinary biomarkers reflecting ferroptosis-related tubular injury remain limited. This study investigated whether urinary retinol-binding protein 4 (RBP4) reflects tubular ferroptosis in DKD. - Source: PubMed
Publication date: 2026/09/28
Jia RuoyuTan RongQian BinTang BihuiZhong YongzhongYu HuiQiao ZiyangMa LeiLi LiminZeng Caihong