CD71
- Known as:
- CD71
- Catalog number:
- 1D-353-T100
- Product Quantity:
- 100 tests
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD71
Related genes to: CD71
- Gene:
- TFRC NIH gene
- Name:
- transferrin receptor
- Previous symbol:
- -
- Synonyms:
- CD71, TFR1, p90
- Chromosome:
- 3q29
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2014-11-19
Related products to: CD71
Related articles to: CD71
- Ischemic stroke remains a leading cause of mortality and disability worldwide, yet current therapeutic strategies, such as thrombolysis and thrombectomy, are constrained by narrow treatment windows and incomplete microvascular repair. While angiogenesis is pivotal for long-term functional recovery, the epigenetic mechanisms governing post-stroke vascular remodeling remain poorly understood. Here, we demonstrate that the long non-coding RNA (lncRNA) Malat1 acts as a critical endothelial regulator of angiogenesis and neurological restoration. Using an endothelium-specific Malat1 overexpression mouse model (EC-Malat1 Tg), we demonstrate endothelial Malat1 upregulation enhances angiogenesis, restores cerebral blood flow, and improves sensorimotor and cognitive function following ischemic stroke. Mechanistically, fluorescence-activated cell sorting (FACS)-based RNA sequencing of brain endothelial cells identified novel downstream targets of Malat1, including Hapln2, Bcl6, Esr1, Sox17, Tfrc, Hsp90aa1, and Tek. Among these, Tek (Tie2) showed robust endothelial co-localization and direct interaction with Malat1. Notably, while Malat1 overexpression markedly increased Tek protein expression, adeno-associated virus (AAV)-mediated endothelial knockdown of Tek abrogated the pro-angiogenic and neurovascular reparative effects of Malat1. Collectively, our data establishes the Malat1-Tek axis as a novel signaling pathway essential for driving post-ischemic cerebrovascular remodeling and long-term functional recovery. Targeting Malat1 represents a novel restorative therapeutic approach for ischemic stroke. - Source: PubMed
Publication date: 2026/10/01
Xiong TianqingZhang MengqiSun PingZhang YuchiNi AndrewZhang ShiqingZhang YuxinHuang XinleiQiu NaLi ShunSun DandanYin Ke-Jie - Effective treatment of ischemic stroke requires improved perfusion and drug delivery to the ischemic penumbra. We investigated whether sensory stimulation could enhance cerebral blood flow and improve delivery of an apoferritin (Aft)-based ginsenoside Rb1 nanodelivery system (Aft@Rb1). Sensory stimulation increased blood flow in the barrel cortex after cerebral ischemia-reperfusion (I/R). By exploiting increased transferrin receptor 1 expression in cerebrovascular endothelial cells, Aft@Rb1 achieved targeted delivery to ischemic tissue. In mice with cerebral I/R, sensory stimulation combined with Aft@Rb1 increased local Rb1 accumulation, reduced blood-brain barrier disruption and infarct area, and improved neurological recovery. These findings indicate that sensory stimulation can enhance local perfusion and nanodrug delivery, providing a potential combined therapeutic strategy for ischemic brain injury. - Source: PubMed
Publication date: 2026/09/29
Wang QiOuyang RuiHu FangboFeng JieJia GuangyuTang XiaolongCui YajingJiang JingjingLi YuhengWu LeiLi ShiyongWang Ye - 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 - Radiation-induced oral mucositis (RIOM) is the most common complication in patients receiving radiotherapy for head and neck, to which ferroptosis is an important contributor. Transferrin receptor (TFRC) -mediated endocytosis is a critical source of iron. Accordingly, we proposed that inhibiting ferroptosis by disrupting TFRC mediated-iron uptake. In this study, we developed endosome-targeting self-assembling nanoparticles (CB NPs) integrated into a detachable microneedle patch (CBT@MNs) for precise and synergistic RIOM therapy. This system integrated the clinically conventional drugs chloroquine and baicalin and loaded into MN patch for mucosal drug delivery. In the tongue mucosa, the MN tips released CB NPs. Upon entering endosomes through the endocytosis pathway, CB NPs disrupted endosomal acidification through the proton sponge effect, which may block TFRC recycling, achieving long-term inhibition of ferroptosis and inflammation efficacy. In rat models of RIOM, CBT@MNs dramatically attenuated mucosal ulceration and accelerated healing via anti-inflammation, angiogenesis, and collagen deposition. Transcriptomic analysis further revealed that CBT@MNs suppressed ferroptosis and inflammatory signaling. This radioprotective strategy for inhibiting ferroptosis and regulating redox homeostasis provided a novel approach for designing tissue engineering materials. - Source: PubMed
Publication date: 2026/09/03
Xiao YanxuanSun PengchengXu WenjieHao XinyanTang TiantianLiu XinyingHuang HaiGong ZhaojianWu Junyong - The discovery of ferroptosis and cuproptosis has significantly expanded the landscape of programmed cell death. Artesunate (ART), a semisynthetic derivative of artemisinin, exhibits pleiotropic pharmacological activities beyond its canonical antimalarial role, including anticancer and neuroprotective effects. However, a comprehensive review systematically integrating ART's roles in modulating both ferroptosis and cuproptosis remains lacking. This review bridges this gap by synthesizing recent advances. The distinct core mechanisms of ferroptosis and cuproptosis are first outlined. Extensive evidence is then summarized regarding ART-induced ferroptosis in cancers, primarily through disrupting iron homeostasis (e.g., stabilizing transferrin receptor (), promoting ferritinophagy) and impairing antioxidant defenses (e.g., suppressing the System Xc/ glutathione peroxidase 4 (GPX4) axis, targeting peroxiredoxins). In contrast, the anti-cuproptotic effect of ART is currently restricted to Parkinson's disease (PD) models, mediated by the upregulation of astrocytic metallothionein 2A (MT2A) to chelate excess copper-the only validated cuproptosis-related mechanism of ART to date. The crosstalk between ferroptosis and cuproptosis at shared metabolic nodes, including glutathione depletion, mitochondrial dysfunction, and reactive oxygen species (ROS) amplification, is further delineated as a hypothesis-generating framework. This interplay suggests a theoretical potential for ART-when combined with functional nano-materials-to synchronously engage both death pathways, though direct experimental validation of such dual-pathway synergy for ART as a single agent remains lacking. Finally, translational prospects of ART in cancer therapy, neurodegenerative diseases, and hepatic fibrosis are discussed, together with current challenges and future directions. ART acts as a context-dependent modulator: pro-ferroptotic activity is evident across multiple disease models, whereas anti-cuproptotic activity is currently limited to PD and requires further validation. Systematic characterization of ART's context-specific effects suggests a preclinical rationale for the future design of ART-based combination strategies targeting metal-dependent cell death, pending further validation. - Source: PubMed
Publication date: 2026/09/02
Feng KaiXia YayiLiu JingshengYang Mingxuan