We are analyzing https://link.springer.com/article/10.1007/s10787-025-01672-7.

Title:
Ferroptosis role in complexity of cell death: unrevealing mechanisms in Parkinson’s disease and therapeutic approaches | Inflammopharmacology
Description:
Parkinson’s disease (PD), a common neurodegenerative disorder, is characterized by progressive loss of dopaminergic neurons, and accumulation of α-synuclein in the substantial nigra. Emerging evidence identifies ferroptosis as a regulated iron-dependent cell death mechanism marked by excessive lipid peroxidation (LPO) as a key contributor to PD pathogenesis. Ferroptosis is intertwined with critical disease processes such as aggregation of α-synuclein protein, oxidative stress generation, mitochondrial alteration, iron homeostasis dysregulation, and neuroinflammation. This mechanism disrupts cellular homeostasis by impairing iron metabolism and antioxidant pathways like the xc−/glutathione/GPX4 axis and the CoQ10 pathway. This review consolidates current advancements in understanding ferroptosis in these mechanisms, increasing interest in contribution to PD pathology. In addition, it explores the latest developments in ferroptosis-targeting pharmacological agents, including their application in the preclinical and clinical study, and highlights their potential to revolutionize PD management. Unraveling the interplay between ferroptosis and PD offers a transformative perspective, paving the way for innovative therapies to combat this debilitating disease condition.
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Keywords {🔍}

pubmed, article, google, scholar, cas, disease, central, parkinsons, ferroptosis, cell, iron, httpsdoiorgs, death, wang, lipid, mechanisms, mol, therapeutic, peroxidation, diseases, zhang, brain, neurodegenerative, protein, sci, kim, liu, yang, role, clinical, med, neurodegeneration, signal, model, chen, data, review, health, res, neurosci, redox, huang, tang, stockwell, jiang, biol, singh, emerging, oxidative, antioxidant,

Topics {✒️}

month download article/chapter dopamine transporter fp-cit-spect α-synuclein-induced cell death montes-de-oca-luna transfusion-dependent beta-thalassemia open-label extension study cortex-derived hepcidin expression β-amyloid precursor protein mptp-induced monkey model ferroptosis-targeting pharmacological agents polyunsaturated fatty acids ether-phospholipid membrane composition brca-proficient ovarian cancer article inflammopharmacology aims full article pdf kousik maparu authored radical-trapping antioxidant activity xc−/glutathione/gpx4 axis treat ferroptosis-related diseases iron homeostasis dysregulation sk-n-mc cells shamsher singh conceived menadione-induced damage dopaminergic neuronal death alpha-synuclein toxicity privacy choices/manage cookies α-synuclein protein mir-335 promotes ferroptosis finkelstein di article awasthi regulated cell death brain iron chelation castillo-quan ji dynamin-related protein 1 nigral cell death iron-dependent form inhibits ferroptosis induced alpha-synuclein protein de souza nogueira de melo lb mptp-treated mice iron regulatory protein increased brain iron pacheco-moisés fp pastor-maldonado cj de freitas fa excessive lipid peroxidation decreasing lipid peroxidation lowering lipid peroxidation article log

Questions {❓}

Feng H, Stockwell BR (2018) Unsolved mysteries: how does lipid peroxidation cause ferroptosis?
Wiciński M, Liczner G, Cadelski K, Kołnierzak T, Nowaczewska M, Malinowski B (2020) Anemia of chronic diseases: wider diagnostics-better treatment?

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         description:Parkinson’s disease (PD), a common neurodegenerative disorder, is characterized by progressive loss of dopaminergic neurons, and accumulation of α-synuclein in the substantial nigra. Emerging evidence identifies ferroptosis as a regulated iron-dependent cell death mechanism marked by excessive lipid peroxidation (LPO) as a key contributor to PD pathogenesis. Ferroptosis is intertwined with critical disease processes such as aggregation of α-synuclein protein, oxidative stress generation, mitochondrial alteration, iron homeostasis dysregulation, and neuroinflammation. This mechanism disrupts cellular homeostasis by impairing iron metabolism and antioxidant pathways like the xc−/glutathione/GPX4 axis and the CoQ10 pathway. This review consolidates current advancements in understanding ferroptosis in these mechanisms, increasing interest in contribution to PD pathology. In addition, it explores the latest developments in ferroptosis-targeting pharmacological agents, including their application in the preclinical and clinical study, and highlights their potential to revolutionize PD management. Unraveling the interplay between ferroptosis and PD offers a transformative perspective, paving the way for innovative therapies to combat this debilitating disease condition.
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      description:Parkinson’s disease (PD), a common neurodegenerative disorder, is characterized by progressive loss of dopaminergic neurons, and accumulation of α-synuclein in the substantial nigra. Emerging evidence identifies ferroptosis as a regulated iron-dependent cell death mechanism marked by excessive lipid peroxidation (LPO) as a key contributor to PD pathogenesis. Ferroptosis is intertwined with critical disease processes such as aggregation of α-synuclein protein, oxidative stress generation, mitochondrial alteration, iron homeostasis dysregulation, and neuroinflammation. This mechanism disrupts cellular homeostasis by impairing iron metabolism and antioxidant pathways like the xc−/glutathione/GPX4 axis and the CoQ10 pathway. This review consolidates current advancements in understanding ferroptosis in these mechanisms, increasing interest in contribution to PD pathology. In addition, it explores the latest developments in ferroptosis-targeting pharmacological agents, including their application in the preclinical and clinical study, and highlights their potential to revolutionize PD management. Unraveling the interplay between ferroptosis and PD offers a transformative perspective, paving the way for innovative therapies to combat this debilitating disease condition.
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