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更新于：2025-05-07

FTMT

更新于：2025-05-07

基本信息

别名

ferritin mitochondrial、Ferritin, mitochondrial、FTMT

+ [1]

简介

Catalyzes the oxidation of ferrous iron(II) to ferric iron(III) and stores iron in a soluble, non-toxic, readily available form (PubMed:11323407, PubMed:15201052). Important for iron homeostasis (PubMed:11323407, PubMed:15201052). Iron is taken up in the ferrous form and deposited as ferric hydroxides after oxidation (PubMed:11323407, PubMed:15201052).

关联

项与 FTMT 相关的药物

DeFer-3

靶点

FTMT

作用机制

FTMT inhibitors

在研机构

University of Wisconsin Madison

原研机构

University of Wisconsin Madison

在研适应症

肿瘤

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

DeFer-2

靶点

FTMT

作用机制

FTMT inhibitors

在研机构

University of Wisconsin Madison

原研机构

University of Wisconsin Madison

在研适应症

肿瘤

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

DeFer-1

靶点

FTMT

作用机制

FTMT inhibitors

在研机构

University of Wisconsin Madison

原研机构

University of Wisconsin Madison

在研适应症

肿瘤

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 FTMT 相关的临床结果

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100 项与 FTMT 相关的转化医学

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0 项与 FTMT 相关的专利（医药）

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125

项与 FTMT 相关的文献（医药）

2025-08-01·Neuropharmacology

Targeting mitochondria-regulated ferroptosis: A new frontier in Parkinson's disease therapy

Review

作者: Liu, Kezhi ; Yang, You ; Xiao, Ruyue ; Li, Xiang ; Guo, Qulian ; Thomas, Elizabeth Rosalind ; Chen, Tianshun ; Wang, Wenjun

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantial nigra. Mitochondrial dysfunction and mitochondrial oxidative stress are central to the pathogenesis of PD, with recent evidence highlighting the role of ferroptosis - a type of regulated cell death dependent on iron metabolism and lipid peroxidation. Mitochondria, the central organelles for cellular energy metabolism, play a pivotal role in PD pathogenesis through the production of Reactive oxygen species (ROS) and the disruption of iron homeostasis. This review explores the intricate interplay between mitochondrial dysfunction and ferroptosis in PD, focusing on key processes such as impaired electron transport chain function, tricarboxylic acid (TCA) cycle dysregulation, disruption of iron metabolism, and altered lipid peroxidation. We discuss key pathways, including the role of glutathione (GSH), mitochondrial ferritin, and the regulation of the mitochondrial labile iron pool (mLIP), which collectively influence the susceptibility of neurons to ferroptosis. Furthermore, this review emphasizes the importance of mitochondrial quality control mechanisms, such as mitophagy and mitochondrial biogenesis, in mitigating ferroptosis-induced neuronal death. Understanding these mechanisms linking the interplay between mitochondrial dysfunction and ferroptosis may pave the way for novel therapeutic approaches aimed at preserving mitochondrial integrity and preventing neuronal loss in PD.

2025-07-01·Cellular Signalling

Mitochondrial ferritin inhibition aggravates pacing-induced ventricular arrhythmias after myocardial infarction by promoting cardiomyocyte ferroptosis

Article

作者: Wang, Yanpeng ; Li, Shuai ; Chang, Yuchen ; Wang, Xiaoqing ; Li, Jingbo ; Huang, Dong ; Chen, Kankai

BACKGROUNDPost-myocardial infarction ventricular arrhythmias are a leading cause of sudden cardiac death (SCD) following acute myocardial infarction worldwide. Emerging evidence suggests that ferroptosis, an iron-dependent form of cell death, plays a significant role in myocardial infarction damage. While mitochondrial ferritin (FtMt) is known to encapsulate harmful ferrous ions within mitochondria, its role in the development of post-myocardial infarction ventricular arrhythmias (post-MI VAs) is not well understood.OBJECTIVEThis study aimed to clarify the role and mechanisms by which FtMt-mediated ferroptosis influences susceptibility to post-MI VAs.METHODSMice were subjected to permanent ligation of the left anterior descending artery (LAD) to induce myocardial infarction (MI), followed by intracardiac electrophysiological studies to evaluate their vulnerability to post-MI VAs. Patch-clamp recordings and confocal Ca²⁺ imaging provided data on neonatal rat ventricular myocytes (NRVMs). We utilized DCFH-DA staining, transmission electron microscopy, and Seahorse analysis to examine the mitochondrial bioenergetics and oxidative phosphorylation in NRVMs.RESULTSFerroptosis was activated in mice post-MI. Inhibiting ferroptosis enhanced cardiac function and reduced the incidence of post-MI VAs. Hypoxia led to electrophysiological dysregulation in NRVMs, which was exacerbated by FtMt inhibition. Specifically, FtMt inhibition under hypoxic conditions further impaired mitochondrial bioenergetics and oxidative phosphorylation, promoting ferroptosis in NRVMs.CONCLUSIONFtMt plays a crucial protective function in MI by limiting infarct size, decreasing the frequency of ventricular arrhythmias, and inhibiting ferroptosis both in vivo and in vitro. These results suggest that FtMt may be a viable therapeutic target for treating MI.

2025-03-01·Journal of Cerebral Blood Flow & Metabolism

Mitochondrial ferritin upregulation by deferiprone reduced neuronal ferroptosis and improved neurological deficits via NDRG1/Yap pathway in a neonatal rat model of germinal matrix hemorrhage

Article

作者: Zhu, Shiyi ; Yang, Xiao ; Xie, Zongyi ; Tang, Jiping ; Li, Ruihao ; Zhang, Xingyu ; Han, Mingyang ; Tao, Yihao ; Chen, Xionghui ; He, Qiuguang ; Yuan, Ye ; Dong, Siyuan ; Kanamaru, Hideki ; Flores, Jerry J ; Zhao, Yutong ; Wu, Lei ; Gu, Lingui ; Zhang, John H ; Yi, Kun ; Huang, Lei

Ferroptosis contributes to brain injury after germinal matrix hemorrhage (GMH). Mitochondrial ferritin (FTMT), a novel mitochondrial outer membrane protein, reduces oxidative stress in neurodegenerative diseases. In vitro, Deferiprone has been shown to upregulate FTMT. However, the effects of FTMT upregulation by Deferiprone on neuronal ferroptosis after GMH and its underlying mechanism has not been investigated. In our study, 389 Sprague-Dawley rat pups of postnatal day 7 were used to establish a collagenase-induced GMH model and an iron-overload model of intracerebral FeCl2 injection. The brain expressions of FTMT, N-myc downstream-regulated gene-1 (NDGR1), Yes-associated protein (YAP), ferroptosis-related molecules including transferrin receptor (TFR) and acyl-CoA synthase long-chain family member 4 (ACSL4) were increased after GMH. FTMT agonist Deferiprone improved neurological deficits and hydrocephalus after GMH. Deferiprone or Adenovirus-FTMT enhanced YAP phosphorylation at the Ser127 site and attenuated ferroptosis, which was reversed by NDRG1 CRISPR Knockout. Iron overload induced neuronal ferroptosis and neurological deficits, which were improved by YAP CRISPR Knockout. Collectively, FTMT upregulation by Deferiprone reduced neuronal ferroptosis and neurological deficits via the NDRG1/YAP signaling pathway after GMH. Deferiprone may serve as a potential non-invasive treatment for GMH patients.

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