The crosstalk between exosomal miRNA and ferroptosis: A narrative review DOI
Zahra Nashtahosseini, Masoumeh Nejatollahi, Ahmad Fazilat

et al.

Biology of the Cell, Journal Year: 2025, Volume and Issue: 117(1)

Published: Jan. 1, 2025

Ferroptosis is a type of cell death that multiple mechanisms and pathways contribute to the positive negative regulation it. For example, increased levels reactive oxygen species (ROS) induce ferroptosis. ferroptosis unlike apoptosis, it not dependent on caspases, but iron. Exosomes are membrane-bound vesicles with size about 30 150 nm, contain various cellular components, including DNA, RNA, microRNAs (miRNAs), lipids, proteins, which genetically similar their cells origin. found in all bodily fluids, blood, saliva, urine. Cells often release exosomes after fusion membrane. They play an important role immune cell-cell communication. miRNAs, noncoding RNAs length 18 24 nucleotides, involved regulating gene expression transcription. Emerging data suggests exosomal miRNAs implicated pathophysiological cells, metastasis, drug resistance, death. In addition, functional studies have indicated can key modulation by Therefore, this review, given importance ferroptosis, we decided elucidate relationship between diseases.

Language: Английский

NCOA4-Mediated Ferritinophagy: A Potential Link to Neurodegeneration DOI Creative Commons
Maria Quiles del Rey, Joseph D. Mancias

Frontiers in Neuroscience, Journal Year: 2019, Volume and Issue: 13

Published: March 14, 2019

NCOA4 (Nuclear receptor coactivator 4) mediates the selective autophagic degradation of ferritin, cellular cytosolic iron storage complex, thereby playing a critical role in intracellular and systemic homeostasis. Disruptions homeostasis autophagy are observed several neurodegenerative disorders raising possibility that NCOA4-mediated ferritinophagy links these two observations may underlie, part, pathophysiology neurodegeneration. Here, we review available evidence detailing molecular mechanisms recent studies examining its erythropoiesis. We propose additional to examine potential brain context diseases.

Language: Английский

Citations

182
Nuclear receptor coactivator 4-mediated ferritinophagy contributes to cerebral ischemia-induced ferroptosis in ischemic stroke DOI
Chong Li, Guangchi Sun, Binglin Chen

et al.

Pharmacological Research, Journal Year: 2021, Volume and Issue: 174, P. 105933 - 105933

Published: Oct. 9, 2021

Language: Английский

Citations

175
Iron, Ferritin, Hereditary Ferritinopathy, and Neurodegeneration DOI Creative Commons

Barry B. Muhoberac,

Rubén Vidal

Frontiers in Neuroscience, Journal Year: 2019, Volume and Issue: 13

Published: Dec. 11, 2019

Cellular growth, function and protection require proper iron management, ferritin plays a physiologically crucial role as the major sequestration storage protein. Ferritin is 24 subunit spherical shell protein composed of both light (FTL) heavy chain (FTH1) subunits, possessing complimentary iron-handling functions forming pores 3-fold 4-fold symmetry. Iron uptake through well-defined, but unloading process somewhat less generally focuses on lysosomal degradation although it may have an additional, energetically efficient pore mechanism. Hereditary Ferritinopathy (HF) or neuroferritinopathy autosomal dominant neurodegenerative disease caused by mutations in FTL C-terminal sequence, which turn cause disorder unraveling at allowing leakage enhanced formation toxic, improperly coordinated (ICI). Histopathologically, HF characterized deposition inclusion bodies (IBs) cells overexpress attempt to address accumulation while lacking ability clear its aggregates. Overexpression IB tax materially energetically, i.e., their synthesis disposal systems, hinder cellular transport other spatially dependent functions. ICI causes damage proteins lipids reactive oxygen species (ROS) because high levels brain oxygen, reductants general metabolism, taxing repair. can aggregation indirectly ROS-induced modification destabilization, more directly with mutant bridging. release are also linked misfunction ferritinophagy, sufficient initiate unique programmed cell death ferroptosis causing ROS lipid peroxidation. But buildup suggests suppressed elevated from together leading long-term ferroptotic-like state HF. Several these processes parallels line mouse models. This review addresses roles structure within above-mentioned framework, they relate associated disorders abnormal accumulation, aggregation, oxidative damage, resulting contributions cumulative stress death.

Language: Английский

Citations

153
New Insights into the Role of Ferritin in Iron Homeostasis and Neurodegenerative Diseases DOI
Na Zhang,

Xiao‐Qi Yu,

Junxia Xie

et al.

Molecular Neurobiology, Journal Year: 2021, Volume and Issue: 58(6), P. 2812 - 2823

Published: Jan. 28, 2021

Language: Английский

Citations

145
HMOX1 upregulation promotes ferroptosis in diabetic atherosclerosis DOI

Zhijun Meng,

Hongping Liang, Jianli Zhao

et al.

Life Sciences, Journal Year: 2021, Volume and Issue: 284, P. 119935 - 119935

Published: Sept. 8, 2021

Language: Английский

Citations

142
Regulation of tissue iron homeostasis: the macrophage “ferrostat” DOI Creative Commons
Nathan C. Winn, Katrina M. Volk, Alyssa H. Hasty

et al.

JCI Insight, Journal Year: 2020, Volume and Issue: 5(2)

Published: Jan. 29, 2020

Iron is an essential element for multiple fundamental biological processes required life; yet iron overload can be cytotoxic. Consequently, concentrations at the cellular and tissue level must exquisitely governed by mechanisms that complement fine-tune systemic control. It well appreciated macrophages are vital homeostasis, supplying or sequestering as needed erythropoiesis bacteriostasis, respectively. Indeed, recycling of through erythrophagocytosis splenic a major contributor to homeostasis. However, accumulating evidence suggests tissue-resident regulate local availability modulate microenvironment, contributing function. Here, we summarize significance tissue-specific regulation highlight how resident critical this process. This tissue-dependent has broad implications understanding both macrophage function homeostasis in health disease.

Language: Английский

Citations

139
HMGB1 regulates ferroptosis through Nrf2 pathway in mesangial cells in response to high glucose DOI Open Access
You Wu, Ying Zhao,

Han-Ze Yang

et al.

Bioscience Reports, Journal Year: 2021, Volume and Issue: 41(2)

Published: Feb. 1, 2021

Abstract Ferroptosis, a novel type of programmed cell death, is involved in inflammation and oxidation various human diseases, including diabetic kidney disease. The present study explored the role high-mobility group box-1 (HMGB1) on regulation ferroptosis mesangial cells response to high glucose. Compared with healthy control, levels serum ferritin, lactate dehydrogenase (LDH), reactive oxygen species (ROS), malonaldehyde (MDA), HMGB1 were significantly elevated nephropathy (DN) patients, accompanied deregulated ferroptosis-related molecules, long-chain acyl-CoA synthetase 4 (ACSL4), prostaglandin-endoperoxide synthase 2 (PTGS2), NADPH oxidase 1 (NOX1), glutathione peroxidase (GPX4). In vitro assay revealed that erastin glucose both induced cells. Suppression restored cellular proliferation, prevented ROS LDH generation, decreased ACSL4, PTGS2, NOX1, increased GPX4 Furthermore, nuclear factor E2-related (Nrf2) was DN patients glucose-mediated translocation Knockdown suppressed glucose-induced activation TLR4/NF-κB axis promoted Nrf2 expression as well its downstream targets HO-1, NQO-1, GCLC, GCLM. Collectively, these findings suggest regulates via pathway

Language: Английский

Citations

137
Ferroptosis and NRF2: an emerging battlefield in the neurodegeneration of Alzheimer's disease DOI
Darius J.R. Lane,

Billie Metselaar,

Mark Greenough

et al.

Essays in Biochemistry, Journal Year: 2021, Volume and Issue: 65(7), P. 925 - 940

Published: Oct. 10, 2021

Ferroptosis is an iron- and lipid peroxidation-dependent cell death modality emerging evidence indicates that ferroptosis has great explanatory potential for neuronal loss associated CNS dysfunction in a range of neurodegenerative diseases (e.g., Alzheimer's, Parkinson's Huntington's diseases, Motor neuron disease, Friedreich ataxia (FRDA)). Ferroptotic results from lethal levels phospholipid hydroperoxides are generated by iron-dependent peroxidation polyunsaturated fatty acids (PUFAs), such as arachidonic adrenic acids, which conjugated to specific phospholipids phosphatidylethanolamines (PEs)). The major cellular protector against glutathione peroxidase 4 (GPX4), membrane-associated selenoenzyme reduces deleterious their corresponding benign alcohols glutathione-dependent manner. Other complementary protective systems have also been identified act bolster defences ferroptosis. Many pharmacological modulators the pathway identified, targeting proteins involved iron homoeostasis autophagy; production detoxification peroxides, cyst(e)ine/glutathione metabolism. While growing number signalling pathways converge regulate cascade, understanding regulation suggests ferroptotic 'tone' cells can be set transcription factor, nuclear factor erythroid 2-related 2 (NRF2), transcriptionally controls many key components pathway. In this review, we provide critical overview relationship between NRF2 signalling. With focus on role Alzheimer's disease (AD), discuss how therapeutic modulation viable strategy explore treatment ferroptosis-driven neurodegeneration.

Language: Английский

Citations

113
Autophagy, Pyroptosis, and Ferroptosis: New Regulatory Mechanisms for Atherosclerosis DOI Creative Commons
Lin Lin,

Mu-xin Zhang,

Lei Zhang

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2022, Volume and Issue: 9

Published: Jan. 13, 2022

Atherosclerosis is a chronic inflammatory disorder characterized by the gradual buildup of plaques within vessel wall middle-sized and large arteries. The occurrence development atherosclerosis rupture are related to injury vascular cells, including endothelial smooth muscle macrophages. Autophagy subcellular process that plays an important role in degradation proteins damaged organelles, autophagy cells closely atherosclerosis. Pyroptosis proinflammatory form regulated cell death, while ferroptosis nonapoptotic death involving overwhelming iron-dependent lipid peroxidation. Both them exhibit distinct features from apoptosis, necrosis, morphology, biochemistry, genetics. However, growing body evidence suggests pyroptosis interact with participate cancers, degenerative brain diseases cardiovascular diseases. This review updated current understanding autophagy, pyroptosis, ferroptosis, finding potential links their effects on atherogenesis plaque stability, thus providing ways develop new pharmacological strategies address stabilize vulnerable, ruptured plaques.

Language: Английский

Citations

111
Ferroptosis: regulation by competition between NRF2 and BACH1 and propagation of the death signal DOI Open Access
Hironari Nishizawa, Mie Yamanaka, Kazuhiko Igarashi

et al.

FEBS Journal, Journal Year: 2022, Volume and Issue: 290(7), P. 1688 - 1704

Published: Feb. 2, 2022

Ferroptosis is triggered by a chain of intracellular labile iron-dependent peroxidation cell membrane phospholipids. important not only as cause ischaemic and neurodegenerative diseases but also mechanism cancer suppression, better understanding its regulatory required. It has become clear that ferroptosis finely controlled two oxidative stress-responsive transcription factors, NRF2 (NF-E2-related factor 2) BACH1 (BTB CNC homology 1). inhibit promote ferroptosis, respectively, activating or suppressing the expression genes in major pathways ferroptosis: iron metabolism, GSH (glutathione) -GPX4 (glutathione peroxidase 4) pathway FSP1 (ferroptosis suppressor protein 1)-CoQ (coenzyme Q) pathway. In addition to this, control through regulation lipid metabolism differentiation. This multifaceted considered have been acquired during evolution multicellular organisms, allowing utilization for maintaining homeostasis, including suppression. terms cell-cell interaction, it revealed property propagating surrounding cells along with peroxidation. The propagation phenomenon could be used realize anticancer therapy future. this review, these points will summarized discussed.

Language: Английский

Citations

98