Cell Research, Год журнала: 2025, Номер unknown
Опубликована: Фев. 25, 2025
Язык: Английский
Signal Transduction and Targeted Therapy, Год журнала: 2024, Номер 9(1)
Опубликована: Окт. 14, 2024
Iron, an essential mineral in the body, is involved numerous physiological processes, making maintenance of iron homeostasis crucial for overall health. Both overload and deficiency can cause various disorders human diseases. Ferroptosis, a form cell death dependent on iron, characterized by extensive peroxidation lipids. Unlike other kinds classical unprogrammed death, ferroptosis primarily linked to disruptions metabolism, lipid peroxidation, antioxidant system imbalance. Ferroptosis regulated through transcription, translation, post-translational modifications, which affect cellular sensitivity ferroptosis. Over past decade or so, diseases have been as part their etiology, including cancers, metabolic disorders, autoimmune diseases, central nervous cardiovascular musculoskeletal Ferroptosis-related proteins become attractive targets many major that are currently incurable, some regulators shown therapeutic effects clinical trials although further validation potential needed. Therefore, in-depth analysis its molecular mechanisms may offer additional strategies prevention treatment. In this review, we discuss significance contribution etiology development along with evidence supporting targeting approach. Importantly, evaluate recent promising interventions, providing guidance future targeted treatment therapies against
Язык: Английский
Процитировано
42
Signal Transduction and Targeted Therapy, Год журнала: 2025, Номер 10(1)
Опубликована: Фев. 2, 2025
Язык: Английский
Процитировано
3
International Journal of Medical Sciences, Год журнала: 2025, Номер 22(3), С. 508 - 527
Опубликована: Янв. 1, 2025
Background: Recent research emphasizes the significant regulatory functions of epigenetic alterations and post-translational modifications (PTMs) in ferroptosis process. Despite existing volume literature, there is a remarkable shortage comprehensive analyses that systematically trace evolution research, map key investigative routes, evaluate current situation field, determine central themes, predict future directions. This study intends to offer summary progress achieved during past 12 years comprehending how PTMs regulate ferroptosis. Methods: The dataset originated from Web Science, covering period January 1, 2012, May 21, 2024. By employing advanced analytical tools, we carried out an extensive scientometric assessment combination with detailed visual data analysis. Results: results emphasize crucial role China, which contributes 69.59% global output, thereby demonstrating its influence on trajectory this domain. Remarkable productivity manifested at institutions such as Central South University, Shanghai Jiao Tong Zhejiang University. Liu Shuang Tang Daolin stand most productive authors field. journal Cell Death & Disease leads terms publication volume, having published greatest number articles related area. identified hepatocellular carcinoma, mitochondrial diseases, iron overload prominent diseases explored Conclusion: meticulous beneficial both experienced researchers newcomers by providing essential information facilitating derivation innovative concepts
Язык: Английский
Процитировано
2
Redox Biology, Год журнала: 2024, Номер 75, С. 103259 - 103259
Опубликована: Июнь 27, 2024
Ferroptosis is a form of iron-related oxidative cell death governed by an integrated redox system, encompassing pro-oxidative proteins and antioxidative proteins. These undergo precise control through diverse post-translational modifications, including ubiquitination, phosphorylation, acetylation, O-GlcNAcylation, SUMOylation, methylation, N-myristoylation, palmitoylation, modification. modifications play pivotal roles in regulating protein stability, activity, localization, interactions, ultimately influencing both the buildup iron lipid peroxidation. In mammalian cells, regulators ferroptosis typically degradation via two principal pathways: ubiquitin-proteasome which handles majority degradation, autophagy, primarily targeting long-lived or aggregated This comprehensive review aims to summarize recent advances modification linked ferroptosis. It also discusses strategies for modulating systems, providing new insights into potential therapeutic applications cancer non-neoplastic diseases.
Язык: Английский
Процитировано
13
Cell, Год журнала: 2024, Номер unknown
Опубликована: Ноя. 1, 2024
Язык: Английский
Процитировано
8
Nature Communications, Год журнала: 2025, Номер 16(1)
Опубликована: Фев. 25, 2025
Abstract Cell death programs such as apoptosis and ferroptosis are associated with aberrant redox homeostasis linked to lipid metabolism membrane function. Evidence for cross-talk between these is emerging. Here, we show that cytotoxic stress channels polyunsaturated fatty acids via lysophospholipid acyltransferase 12 into phospholipids become susceptible peroxidation under additional stress. This reprogramming altered acyl-CoA synthetase isoenzyme expression caused by a decrease in growth factor receptor tyrosine kinase (RTK)-phosphatidylinositol-3-kinase signaling, resulting suppressed acid biosynthesis, specific stressors impaired Akt-SREBP1 activation. The reduced availability of de novo synthesized favors the channeling phospholipids. Growth withdrawal serum starvation mimics this phenotype, whereas RTK ligands counteract it. We conclude attenuated signaling during cell initiation increases cells’ susceptibility oxidative damage at interface alternative programs.
Язык: Английский
Процитировано
1
Journal of Neurochemistry, Год журнала: 2025, Номер 169(3)
Опубликована: Март 1, 2025
ABSTRACT Parkinson's disease (PD) is a neurodegenerative disorder that gets exacerbated by vascular injury. Neural stem cell‐derived exosomes (NSC‐Exos) display effective neuroprotective properties in PD models. Cell division control protein 42 (CDC42) connected to angiogenesis, but its effects remain undefined. This research aims reveal the role of CDC42 PD. First, we applied 1‐methyl‐4‐phenylpyridinium (MPP + ) induce human cerebral microvascular endothelial cells (HCMECs) model and evaluated cell viability ferroptosis. Then, characterized NSC‐Exos. Next, appraise effect hypoxia‐pretreated NSC‐Exos (H‐NSC‐Exos) on MPP ‐induced model, examined angiogenesis ferroptosis HCMECs. Moreover, constructed mice using 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) tested behavioral experiments injury mice. Furthermore, cellular after knockdown CDC42. Additionally, investigated interaction with Acyl‐CoA synthetase long‐chain family member 4 (ACSL4) detected overexpression ACSL4. We found H‐NSC‐Exos reversed decrease HCMECs migration, lowered lipid‐reactive oxygen species (lipid‐ROS) levels, suppressed ferroptosis, facilitated angiogenesis. attenuated MPTP‐induced development, injury, reduced raised lipid‐ROS which were ferrostatin‐1 liproxstatin‐1. interacted ACSL4 aggravated above was knocked down. Our study reveals H‐NSC‐Exos‐derived inhibited ACSL4‐related alleviate may serve as potent therapeutic target for treatment. image
Язык: Английский
Процитировано
1
Free Radical Biology and Medicine, Год журнала: 2024, Номер 222, С. 539 - 551
Опубликована: Июль 9, 2024
Oxygen molecules accept electrons from the respiratory chain in mitochondria and are responsible for energy production aerobic organisms. The reactive oxygen species formed via these reduction processes undergo complicated electron transfer reactions with other biological substances, which leads to alterations their physiological functions cause diverse pathophysiological consequences (e.g., oxidative stress). accounts only a small proportion of redox organisms, especially under or hypoxic conditions but not anaerobic conditions. This article discusses completely new concept biology, is governed by redox-active supersulfides, i.e., sulfur-catenated molecular species. These present abundance all organisms remain largely unexplored terms biology life science research. In fact, accumulating evidence shows that supersulfides have extensive chemical properties they can be readily ionized radicalized participate metabolism, signaling, stress responses cells vivo. Thus, pharmacological intervention medicinal modulation supersulfide activities been shown benefit regulation disease pathogenesis as well control.
Язык: Английский
Процитировано
7
Biomolecules, Год журнала: 2024, Номер 14(10), С. 1334 - 1334
Опубликована: Окт. 20, 2024
Inositol 1,4,5-trisphosphate receptors (IP
Язык: Английский
Процитировано
6
Frontiers in Oncology, Год журнала: 2024, Номер 14
Опубликована: Авг. 12, 2024
Ferroptosis is an iron-dependent form of cell death that results from excess lipid peroxidation in cellular membranes. Within the last decade, physiological and pathological roles for ferroptosis have been uncovered autoimmune diseases, inflammatory conditions, infection, cancer biology. Excitingly, metabolism may be targeted to induce by cancers are resistant other forms death. sensitivity regulated oxidative stress, metabolism, iron which all influenced tumor microenvironment (TME). Whereas some types shown adapt these stressors, it not clear how immune cells regulate their sensitivities ferroptosis. In this review, we discuss mechanisms different subsets, influences infiltrate TME, interactions can determine epithelial-to-mesenchymal transition (EMT) metastasis. While much focus has placed on inducing cells, important considerations ferroptosis-modulating strategies impact anti-tumor immunity. From perspective, also promising immunotherapies field challenges associated with targeting specific populations.
Язык: Английский
Процитировано
5