We are analyzing https://link.springer.com/article/10.1007/s13105-025-01078-7.

Title:
Ferroptosis in immune chaos: Unraveling its impact on disease and therapeutic potential | Journal of Physiology and Biochemistry
Description:
Since its introduction in 2012, ferroptosis has garnered significant attention from researchers over the past decade. Unlike autophagy and apoptosis, ferroptosis is an atypical iron-dependent programmed cell death that falls under necrosis. It is regulated by various cellular metabolic and signaling processes, which encompass amino acid, lipid, iron, and mitochondrial metabolism. The initiation of ferroptosis occurs through iron-dependent phospholipid peroxidation. Notably, ferroptosis exhibits a dual effect and is associated with various diseases. A significant challenge lies in managing autoimmune disorders with unknown origins that stem from the reactivation of the immune system. Two contributing factors to autoimmunity are the aberrant stimulation of cell death and the inadequate clearance of dead cells, which can expose or release intracellular components that activate the immune response. Ferroptosis is distinct from other forms of cell death, such as apoptosis, necroptosis, autophagy, and pyroptosis, due to its unique morphological, biochemical, and genetic characteristics and specific relationship with cellular iron levels. Recent studies indicate that immune cells can both induce and undergo ferroptosis. To better understand how ferroptosis influences immune responses and its imbalance in disease, a molecular understanding of the relationship between ferroptosis and immunity is essential. Consequently, further research is needed to develop immunotherapeutics that target ferroptosis. This review primarily focuses on the role of ferroptosis in immune-related disorders.
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Keywords {🔍}

pubmed, article, google, scholar, cas, ferroptosis, central, cell, death, disease, iron, chen, liu, cancer, wang, cells, biol, med, nat, role, mol, zhang, nature, yang, diseases, arthritis, lipid, chem, patients, int, sci, rev, multiple, immunol, dis, regulation, front, res, apoptosis, metabolism, rheumatoid, mechanisms, zhou, cellular, autoimmune, sclerosis, immune, therapeutic, autophagy, pyroptosis,

Topics {✒️}

month download article/chapter er-stress-related perk pathway mitochondrial ros-autophagy-lysosomal pathway iron-dependent phospholipid peroxidation salmonella-induced caspase-2 activation p53/nrf2/slc7a11 pathway arsenic trioxide-mediated apoptosis ragulator-rag-mtorc1 pathway α-synuclein preformed fibrils caspase-1–dependent mitochondrial damage serum oxidant/antioxidant status nucleic acid–binding activities single-cell transcriptome level prevent hydroperoxide-induced ferroptosis nrf2/ho-1 signaling pathway genotype-selective antitumor agents dhodh-mediated ferroptosis defence relapsing-remitting multiple sclerosis dose-dependent protective effect glutathione-independent ferroptosis suppressor naf-1-deficient pancreatic cells free radical-lipid interactions p53-mediated tumour suppression systemic lupus erythematosus central neurological disorders placebo-controlled pilot study oxidative/anti-oxidative status α-synuclein raav parkinson lipid peroxidase pathway full article pdf activates inflammasome-ferroptosis processes deferoxamine induced decreases insulin secretion dysfunction iron-dependent form double-edged sword oral n-acetylcysteine di stasi lc polyunsaturated fatty acids reactive oxygen species joint-specific gene expression multiple sclerosis-relevant regulator gpx4 mediated suppression programmed cell death experimental autoimmune encephalomyelitis therapy-resistant state privacy choices/manage cookies placebo-controlled trial van leyen kjbeba lethal polymicrobial sepsis omega-3 fatty acids

Questions {❓}

Diggle CPJPiLR (2002) In vitro studies on the relationship between polyunsaturated fatty acids and cancer: tumour or tissue specific effects?
De Oliveira ECS, Quaglio AEV, Grillo TG, Di Stasi LC, Sassaki LY (2024) MicroRNAs in inflammatory bowel disease: What do we know and what can we expect?

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         description:Since its introduction in 2012, ferroptosis has garnered significant attention from researchers over the past decade. Unlike autophagy and apoptosis, ferroptosis is an atypical iron-dependent programmed cell death that falls under necrosis. It is regulated by various cellular metabolic and signaling processes, which encompass amino acid, lipid, iron, and mitochondrial metabolism. The initiation of ferroptosis occurs through iron-dependent phospholipid peroxidation. Notably, ferroptosis exhibits a dual effect and is associated with various diseases. A significant challenge lies in managing autoimmune disorders with unknown origins that stem from the reactivation of the immune system. Two contributing factors to autoimmunity are the aberrant stimulation of cell death and the inadequate clearance of dead cells, which can expose or release intracellular components that activate the immune response. Ferroptosis is distinct from other forms of cell death, such as apoptosis, necroptosis, autophagy, and pyroptosis, due to its unique morphological, biochemical, and genetic characteristics and specific relationship with cellular iron levels. Recent studies indicate that immune cells can both induce and undergo ferroptosis. To better understand how ferroptosis influences immune responses and its imbalance in disease, a molecular understanding of the relationship between ferroptosis and immunity is essential. Consequently, further research is needed to develop immunotherapeutics that target ferroptosis. This review primarily focuses on the role of ferroptosis in immune-related disorders.
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      headline:Ferroptosis in immune chaos: Unraveling its impact on disease and therapeutic potential
      description:Since its introduction in 2012, ferroptosis has garnered significant attention from researchers over the past decade. Unlike autophagy and apoptosis, ferroptosis is an atypical iron-dependent programmed cell death that falls under necrosis. It is regulated by various cellular metabolic and signaling processes, which encompass amino acid, lipid, iron, and mitochondrial metabolism. The initiation of ferroptosis occurs through iron-dependent phospholipid peroxidation. Notably, ferroptosis exhibits a dual effect and is associated with various diseases. A significant challenge lies in managing autoimmune disorders with unknown origins that stem from the reactivation of the immune system. Two contributing factors to autoimmunity are the aberrant stimulation of cell death and the inadequate clearance of dead cells, which can expose or release intracellular components that activate the immune response. Ferroptosis is distinct from other forms of cell death, such as apoptosis, necroptosis, autophagy, and pyroptosis, due to its unique morphological, biochemical, and genetic characteristics and specific relationship with cellular iron levels. Recent studies indicate that immune cells can both induce and undergo ferroptosis. To better understand how ferroptosis influences immune responses and its imbalance in disease, a molecular understanding of the relationship between ferroptosis and immunity is essential. Consequently, further research is needed to develop immunotherapeutics that target ferroptosis. This review primarily focuses on the role of ferroptosis in immune-related disorders.
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      name:Pharmacy Department, Tishk International University, Erbil, Iraq
      name:Department of Chemistry and Biochemistry, School of Sciences, JAIN (Deemed to Be University), Bangalore, India
      name:Centre for Research Impact & Outcome, Chitkara University Institute of Engineering and Technology, Chitkara University, Rajpura, India
      name:Department of Biology, College of Education for Pure Sciences, University of Anbar, Ramadi, Iraq
      name:Department of Chemistry, Chandigarh Engineering College, Chandigarh Group of Colleges-Jhanjeri, Mohali, India
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      name:Department of Prosthetic Dentistry, Sechenov First Moscow State Medical University, Moscow, Russia
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