Free Radical Biology and Medicine, Год журнала: 2025, Номер unknown
Опубликована: Май 1, 2025
Язык: Английский
Free Radical Biology and Medicine, Год журнала: 2025, Номер unknown
Опубликована: Май 1, 2025
Язык: Английский
Chemical Engineering Journal, Год журнала: 2025, Номер 505, С. 159676 - 159676
Опубликована: Янв. 17, 2025
Язык: Английский
Процитировано
2Advanced Biology, Год журнала: 2025, Номер unknown
Опубликована: Апрель 9, 2025
Abstract Ferroptosis, as novel type of regulated cell death that has garnered widespread attention over the past decade, witnessed continuous discovery an increasing number regulatory mechanisms. Trace metal elements play a multifaceted and crucial role in oncology. Interestingly, it been increasingly evident these elements, such copper, are involved regulation iron accumulation, lipid peroxidation antiferroptotic systems, suggesting existence “nonferrous” mechanisms ferroptosis. In this review, comprehensive overview composition mechanism ferroptosis is provided. The interaction between copper metabolism (including cuproptosis) cancer, well roles other trace (such zinc, manganese, cobalt, molybdenum) specifically focused. Furthermore, applications nanomaterials based on metals cancer therapy also reviewed potential strategies for co‐targeting cuproptosis explored. Nevertheless, light intricate ambiguous nature interactions, ongoing research essential to further elucidate ferroptosis, thereby facilitating development therapeutic targets approaches treatment.
Язык: Английский
Процитировано
1Biochemical Pharmacology, Год журнала: 2023, Номер 218, С. 115909 - 115909
Опубликована: Ноя. 4, 2023
Язык: Английский
Процитировано
22Clinical Science, Год журнала: 2024, Номер 138(5), С. 235 - 249
Опубликована: Фев. 15, 2024
Abstract Contrast-induced nephropathy (CIN) is a leading cause of hospital-acquired acute kidney injury (AKI). Recently, ferroptosis was reported to be crucial for AKI pathogenesis. Our previous studies indicated antioxidant tetramethylpyrazine (TMP) prevent CIN in vivo. However, whether involved TMP nephroprotective mechanism against unclear. In the present study, we investigated role renal tubular epithelial cell reno-protective effect and molecular mechanisms by which regulates ferroptosis. Classical contrast-medium, Iohexol, used construct models rats HK-2 cells. Results showed that accompanied both vivo vitro, including typical features ferroptosis, Fe2+ accumulation, lipid peroxidation decreased glutathione peroxidase 4 (GPX4). Ferroptosis inhibition classic inhibitors Fer-1 DFO promoted viability reduced intracellular ROS production. Additionally, significantly inhibited dysfunction, biomarkers, prevented production, accumulation increased GPX4 expression. Expressions various proteins associated with iron ion metabolism, transferrin receptor (TFRC), divalent metal transporter 1, iron-responsive element binding protein 2, ferritin heavy chain ferroportin heat shock factor were examined using mechanistic analyses. Among these, TFRC changes most significant after pretreatment. siRNA knockdown plasmid overexpression essential alleviate reduce LDH release, ROS. findings provide insights about potential treating
Язык: Английский
Процитировано
9Antioxidants, 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
9Drug Discovery Today, Год журнала: 2024, Номер 29(4), С. 103920 - 103920
Опубликована: Фев. 17, 2024
Язык: Английский
Процитировано
9Bioorganic & Medicinal Chemistry, Год журнала: 2024, Номер 105, С. 117716 - 117716
Опубликована: Апрель 9, 2024
Язык: Английский
Процитировано
7Phytomedicine, Год журнала: 2025, Номер 139, С. 156472 - 156472
Опубликована: Фев. 5, 2025
Язык: Английский
Процитировано
1Small, Год журнала: 2025, Номер unknown
Опубликована: Март 6, 2025
Renal ischemia-reperfusion (I/R) significantly contributes to acute kidney injury (AKI), causing substantial oxidative stress and metabolic disruptions. Ferroptosis, a Fe2+-dependent form of regulated cell death characterized by lipid peroxide accumulation, is the predominant cause renal I/R (RIRI). Here, carbon dot (C-dot) nanozymes that inhibit ferroptosis regulating Fe2⁺ levels scavenging reactive oxygen species, offering potential treatment for RIRI are reported. C-dots chelate via surface carbonyl, hydroxyl, carboxyl groups reduce free levels, suppress Fenton reaction, limit hydroxyl radical generation. Additionally, scavenge superoxide anions radicals restore redox balance. By targeting kidneys, effectively iron overload peroxidation prevent ferroptotic in male mice model. RNA sequencing (RNA-seq) analysis further confirms crucial roles mitigating stress, preserving homeostasis, downregulating acyl-CoA synthetase long-chain family member 4 (ACSL4) after I/R. This work emphasizes perfect alignment between multifunctional conditions required inhibiting offers an innovative strategy treat effectively.
Язык: Английский
Процитировано
1Current Research in Toxicology, Год журнала: 2024, Номер 7, С. 100181 - 100181
Опубликована: Янв. 1, 2024
Sickle cell disease (SCD) is an inherited hemoglobin disorder marked by red blood sickling, resulting in severe anemia, painful episodes, extensive organ damage, and shortened life expectancy. In SCD, increased iron levels can trigger ferroptosis, a specific type of death characterized reactive oxygen species (ROS) lipid peroxide accumulation, leading to damage impairments. The intricate interplay between iron, inflammation, oxidative stress SCD underscores the necessity thoroughly understanding these processes for development innovative therapeutic strategies. This review highlights importance balancing complex interactions among various factors exploitation knowledge developing novel therapeutics this devastating disease.
Язык: Английский
Процитировано
6