Treatment and prevention of pathological mitochondrial dysfunction in retinal degeneration and in photoreceptor injury DOI Creative Commons
Walter H. Moos, Douglas V. Faller,

Ioannis P. Glavas

и другие.

Biochemical Pharmacology, Год журнала: 2022, Номер 203, С. 115168 - 115168

Опубликована: Июль 12, 2022

Pathological deterioration of mitochondrial function is increasingly linked with multiple degenerative illnesses as a mediator wide range neurologic and age-related chronic diseases, including those genetic origin. Several these diseases are rare, typically defined in the United States an illness affecting fewer than 200,000 people U.S. population, or about one 1600 individuals. Vision impairment due to dysfunction eye prominent feature evident numerous primary common pathophysiology many familiar ophthalmic disorders, macular degeneration, diabetic retinopathy, glaucoma retinopathy prematurity — collection syndromes, disorders significant unmet medical needs. Focusing on metabolic pathway mechanisms, possible roles cuproptosis ferroptosis retinal dysfunction, we shed light potential α-lipoyl-L-carnitine treating diseases. α-Lipoyl-L-carnitine bioavailable mitochondria-targeting lipoic acid prodrug that has shown protecting against degeneration photoreceptor cell loss indications.

Язык: Английский

Epigenetic modification of ferroptosis by non-coding RNAs in cancer drug resistance DOI Creative Commons
Hongquan Wang, Joshua S. Fleishman,

Sihang Cheng

и другие.

Molecular Cancer, Год журнала: 2024, Номер 23(1)

Опубликована: Авг. 27, 2024

Abstract The development of drug resistance remains a major challenge in cancer treatment. Ferroptosis, unique type regulated cell death, plays pivotal role inhibiting tumour growth, presenting new opportunities treating chemotherapeutic resistance. Accumulating studies indicate that epigenetic modifications by non-coding RNAs (ncRNA) can determine vulnerability to ferroptosis. In this review, we first summarize the growth/development. Then, core molecular mechanisms ferroptosis, its upstream regulation, and downstream effects on Finally, review recent advances understanding how ncRNAs regulate ferroptosis from such modulate This aims enhance general ncRNA-mediated regulatory which highlighting ncRNA-ferroptosis axis as key druggable target overcoming

Язык: Английский

Процитировано

15
Cadmium exposure induced neuronal ferroptosis and cognitive deficits via the mtROS-ferritinophagy pathway DOI
Dongmei Wang, Yiran Wu, Xiang Zhou

и другие.

Environmental Pollution, Год журнала: 2024, Номер 349, С. 123958 - 123958

Опубликована: Апрель 13, 2024

Язык: Английский

Процитировано

13
Dysregulation of iron homeostasis and ferroptosis in sevoflurane and isoflurane associated perioperative neurocognitive disorders DOI Creative Commons
Mengrong Miao, Yaqian Han, Yangyang Wang

и другие.

CNS Neuroscience & Therapeutics, Год журнала: 2024, Номер 30(2)

Опубликована: Фев. 1, 2024

In recent years, sevoflurane and isoflurane are the most popular anesthetics in general anesthesia for their safe, rapid onset, well tolerant. Nevertheless, many studies reported neurotoxicity among pediatric aged populations. This effect is usually manifested as cognitive impairment such perioperative neurocognitive disorders. The wide application of during makes safety a major health concern. Evidence indicates that iron dyshomeostasis ferroptosis may establish role isoflurane. However, mechanisms sevoflurane- isoflurane-induced neuronal injury were not fully understood, which poses barrier to treatment its neurotoxicity. We, therefore, reviewed current knowledge on aimed promote better understanding roles

Язык: Английский

Процитировано

9
Butylated Hydroxytoluene (BHT) Protects SH-SY5Y Neuroblastoma Cells from Ferroptotic Cell Death: Insights from In Vitro and In Vivo Studies DOI Creative Commons

Parisa Faraji,

Astrid Borchert, Shahin Ahmadian

и другие.

Antioxidants, Год журнала: 2024, Номер 13(2), С. 242 - 242

Опубликована: Фев. 17, 2024

Ferroptosis is a special kind of programmed cell death that has been implicated in the pathogenesis large number human diseases. It involves dysregulated intracellular iron metabolism and uncontrolled lipid peroxidation, which together initiate ferroptotic signalling pathways leading to cellular suicide. Pharmacological interference with signal transduction may prevent death, thus patients suffering from ferroptosis-related diseases benefit such treatment. Butylated hydroxytoluene (BHT) an effective anti-oxidant frequently used oil chemistry cosmetics free-radical-mediated peroxidation. Since it functions as radical scavenger, previously reported interfere signalling. Here, we show BHT prevents RSL3- ML162-induced cultured neuroblastoma cells (SH-SY5Y) dose-dependent manner. RSL3-induced oxidation membrane lipids normalises inhibition catalytic activity glutathione peroxidase 4. The systemic application rat Alzheimer’s disease model prevented upregulation expression genes. Taken together, these data indicate interferes animal model.

Язык: Английский

Процитировано

9
The molecular mechanism of ferroptosis and its relationship with Parkinson's disease DOI Creative Commons

Yan Su,

Yue Jiao,

Sheng Cai

и другие.

Brain Research Bulletin, Год журнала: 2024, Номер 213, С. 110991 - 110991

Опубликована: Май 31, 2024

Neurodegenerative diseases such as Parkinson's disease (PD) have complex pathogenetic mechanisms. Genetic, age, and environmental factors are all related to PD. Due the unclear pathogenesis of PD lack effective cure methods, it is urgent find new targets for treating patients. Ferroptosis a form cell death that reliant on iron exhibits distinct morphological mechanistic characteristics compared other types death. It encompasses range biological processes, including iron/lipid metabolism oxidative stress. In recent years, research has found ferroptosis plays crucial role in pathophysiological processes neurodegenerative stroke. Therefore, also closely PD, This article reviews core mechanisms elucidates correlation between ferroptosis. addition, compounds emerged years exert anti effects by inhibiting signaling pathway were summarized. I hope further elaborate relationship through review this article, provide strategies developing treatments targeting

Язык: Английский

Процитировано

9
Adiponectin ameliorates traumatic brain injury-induced ferroptosis through AMPK- ACC1 signaling pathway DOI Creative Commons
Yufeng Ge,

Tinghao Wang,

Qing Hu

и другие.

Brain Behavior and Immunity, Год журнала: 2025, Номер unknown

Опубликована: Фев. 1, 2025

Various forms of neuronal death contribute to neurological injury after traumatic brain (TBI), leading irreversible deficits. Among these, ferroptosis is a form regulated cell characterized by the accumulation iron-dependent lipid hydroperoxides and induced incorporation polyunsaturated fatty acids (PUFAs) into cellular membranes. Adiponectin (APN), cytokine secreted adipocytes, have showed neuroprotective effects binding adiponectin receptors (AdipoRs), which are widely expressed in central nervous system. However, role TBI APN-AdipoRs signaling remains unexplored. Our clinical analysis revealed significant correlation between serum levels APN 6-month outcomes patients. Subsequent studies confirmed that TBI-induced was more pronounced knockout mice compared wild-type mice, while additional receptor agonist (AdipoRon) treatment significantly mitigated ferroptosis. Furthermore, AdipoR1 knockdown diminished protective AdipoRon against erastin-induced primary neurons. Correspondingly, neuron-specific conditional (AdipoR1CKO) neurons were susceptible TBI, increased edema lesion volume, exacerbated Mechanically, activation APN-AdipoR1 promoted adenosine monophosphate activated protein kinase (AMPK) -mediated phosphorylation acetyl-CoA carboxylase-1 (ACC1), thus suppressed PUFAs biosynthesis, determines theferroptosissensitivity Taken together, these findings provided compelling evidence for inhibiting AMPK-ACC1.

Язык: Английский

Процитировано

1
Role of iron in brain development, aging, and neurodegenerative diseases DOI Creative Commons
Qiqi Gao, Yiyang Zhou, Yu Chen

и другие.

Annals of Medicine, Год журнала: 2025, Номер 57(1)

Опубликована: Март 4, 2025

It is now understood that iron crosses the blood-brain barrier via a complex metabolic regulatory network and participates in diverse critical biological processes within central nervous system, including oxygen transport, energy metabolism, synthesis catabolism of myelin neurotransmitters. During brain development, distributed throughout brain, playing pivotal role key such as neuronal myelination, neurotransmitter synthesis. In physiological aging, can selectively accumulate specific regions, impacting cognitive function leading to intracellular redox imbalance, mitochondrial dysfunction, lipid peroxidation, thereby accelerating aging associated pathologies. Furthermore, accumulation may be primary contributor neurodegenerative diseases Alzheimer's Parkinson's diseases. Comprehending diseases, utilizing iron-sensitive Magnetic Resonance Imaging (MRI) technology for timely detection or prediction abnormal neurological states, implementing appropriate interventions instrumental preserving normal system function.

Язык: Английский

Процитировано

1
Lipid metabolism in ferroptosis: mechanistic insights and therapeutic potential DOI Creative Commons
Daoyang Sun, Longfei Wang, Yu‐Hsuan Wu

и другие.

Frontiers in Immunology, Год журнала: 2025, Номер 16

Опубликована: Март 11, 2025

Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, plays a pivotal role in various physiological and pathological processes. In this review, we summarize the core mechanisms ferroptosis, emphasizing its intricate connections to metabolism, including fatty acid synthesis, phospholipid remodeling, oxidation dynamics. We further highlight advancements detection technologies, such as fluorescence imaging, lipidomics, vivo PET which have deepened our understanding ferroptotic regulation. Additionally, discuss ferroptosis human diseases, where it acts double-edged sword, contributing cancer while also driving ischemia-reperfusion injury neurodegeneration. Finally, explore therapeutic strategies aimed at either inducing or inhibiting iron chelation, antioxidant modulation, lipid-targeted interventions. By integrating mechanistic insights, disease relevance, potential, review provides comprehensive perspective on crucial interface between metabolism oxidative stress.

Язык: Английский

Процитировано

1
Glyphosate-triggered hepatocyte ferroptosis via suppressing Nrf2/GSH/GPX4 axis exacerbates hepatotoxicity DOI
Jingbo Liu,

Guangcheng Yang,

Hongna Zhang

и другие.

The Science of The Total Environment, Год журнала: 2022, Номер 862, С. 160839 - 160839

Опубликована: Дек. 12, 2022

Язык: Английский

Процитировано

33
TFR2 regulates ferroptosis and enhances temozolomide chemo-sensitization in gliomas DOI Creative Commons
Shiao Tong, Hong Yu, Yang Xu

и другие.

Experimental Cell Research, Год журнала: 2023, Номер 424(1), С. 113474 - 113474

Опубликована: Янв. 23, 2023

Glioma is a common type of brain tumor with high incidence and mortality rates. Iron plays an important role in various physiological pathological processes. entry into the cell promoted by binding transferrin receptor 2 (TFR2) to iron-transferrin complex. This study was designed assess association between TFR2 ferroptosis glioma. Lipid peroxidation levels glioma cells were assessed determination lipid reactive oxygen species (ROS), glutathione content, mitochondrial membrane potential. The effect on TMZ sensitivity examined viability assays, flow cytometry, colony formation assays. We found that Low expression predicted better prognosis for patients. And overexpression production cells, thereby further promoting ferroptosis. could be reversed inhibitors Fer-1 DFO (both ferroptosis). Moreover, potentiated cytotoxic (temozolomide) via activating In conclusion, we induced enhanced gliomas. Our findings might provide new treatment strategy patients improve their prognosis.

Язык: Английский

Процитировано

22