Ferroptosis is a recently identified cell death process in refrigerated beef, and its mediated protein oxidation and cell death may reduce muscle quality, but the mechanism of ferroptosis is unclear. In the study, free iron accumulation reached 19.670 ± 0.482 μg/g after 6 days refrigeration, the levels of apoptosis, ROS, and lipid peroxidation increased significantly (P < 0.05), and muscle tissue cells exhibited typical ferroptosis characteristics. A total of 377 differentially expressed proteins (DEPs) were identified by TMT quantitative proteomics. 15 DEPs, including transferrin, ferritin, glutathione peroxidase (GPX) 4, and heme oxygenase 1, were involved in lipid peroxidation, Fe and Fe conversion, iron ion accumulation, and mitochondrial oxidative stress to induce ferroptosis. In addition, signalling pathways, such as chemical carcinogenesis-ROS, glutathione metabolism, HIF-1, and PPAR may promote ferroptosis by affecting free iron overload and GPX4 inactivation.
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http://dx.doi.org/10.1016/j.foodchem.2023.137596 | DOI Listing |
ACS Appl Mater Interfaces
January 2025
State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, P.R. China.
Ferroptosis is a unique cell death mode that relies on iron and lipid peroxidation (LPO) and is extensively utilized to treat drug-resistant tumor. However, like the other antitumor model, requirement of oxygen limited its application in treating the malignant tumors in anaerobic environments, just as photodynamic therapy, a very promising anticancer therapy. Here, we show that an iridium(III) complex (Ir-dF), which was often used in proton-coupled electron transport (PCET) process, can induce efficient cell death upon photo irradiation, which can be effectively protected by the typical ferroptosis inhibitor Fer-1 but not by the classic iron chelating agents and ROS scavengers.
View Article and Find Full Text PDFAppl Biochem Biotechnol
January 2025
Department of Internal Medicine-Cardiovascular, Guangzhou Twelfth People's Hospital, No.1, Tianqiang Road, Tianhe District, Guangzhou City, Guangdong Province, 510620, China.
Myocardial infarction (MI) is a coronary artery-related disease that seriously threatens human life and is the leading cause of sudden death worldwide, where a lack of nutrients and oxygen leads to an inflammatory response and death of cardiomyocytes. Ferroptosis is a form of non-apoptotic cell death associated with metabolic dysfunction, resulting in abnormal breakdown of glutamine and iron-dependent accumulation of reactive oxygen species (ROS) during metabolism. However, the molecular mechanism of ferroptosis in the pathogenesis of MI and the function of Klotho and KRAS on ferroptosis during MI remain unclear.
View Article and Find Full Text PDFInt J Cardiol Heart Vasc
February 2025
Department of Geriatrics, Peking University Third Hospital, Beijing 100191, PR China.
Background: Ferroptosis is a cell death process that depends on iron and reactive oxygen species. It significantly contributes to cardiovascular diseases. However, its exact role in ischemic cardiomyopathy (ICM) is still unclear.
View Article and Find Full Text PDFInflamm Res
January 2025
Department of Anesthesiology, Critical Care, and Surgery, Duke University School of Medicine, Durham, NC, USA.
Background: Mitochondria generate the adenosine triphosphate (ATP) necessary for eukaryotic cells, serving as their primary energy suppliers, and contribute to host defense by producing reactive oxygen species. In many critical illnesses, including sepsis, major trauma, and heatstroke, the vicious cycle between activated coagulation and inflammation results in tissue hypoxia-induced mitochondrial dysfunction, and impaired mitochondrial function contributes to thromboinflammation and cell death.
Methods: A computer-based online search was performed using the PubMed and Web of Science databases for published articles concerning sepsis, trauma, critical illnesses, cell death, mitochondria, inflammation, coagulopathy, and organ dysfunction.
Ren Fail
December 2025
Department of Nephrology, Shanxi Provincial People's Hospital, The Fifth Clinical Medical College of Shanxi Medical University, Taiyuan, Shanxi, China.
Copper is a vital cofactor in various enzymes, plays a pivotal role in maintaining cell homeostasis. When copper metabolism is disordered and mitochondrial dysfunction is impaired, programmed cell death such as apoptosis, paraptosis, pyroptosis, ferroptosis, cuproptosis, autophagy and necroptosis can be induced. In this review, we focus on the metabolic mechanisms of copper.
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