Ferroptosis and Iron Homeostasis: Molecular Mechanisms and Neurodegenerative Disease Implications DOI Creative Commons
Nurzhan Abdukarimov, Kamilya Kokabi, Jeannette Kunz

et al.

Antioxidants, Journal Year: 2025, Volume and Issue: 14(5), P. 527 - 527

Published: April 28, 2025

Iron dysregulation has emerged as a pivotal factor in neurodegenerative pathologies, especially through its capacity to promote ferroptosis, unique form of regulated cell death driven by iron-catalyzed lipid peroxidation. This review synthesizes current evidence on the molecular underpinnings focusing how disruptions iron homeostasis interact with key antioxidant defenses, such system Xc−-glutathione-GPX4 axis, tip neurons toward lethal oxidative damage. Building these mechanistic foundations, we explore ferroptosis intersects hallmark pathologies Alzheimer’s disease (AD) and Parkinson’s (PD) examine accumulation vulnerable brain regions may fuel disease-specific protein aggregation neurodegeneration. We further surveyed distinct components highlighting role peroxidation enzymes, mitochondrial dysfunction, recently discovered parallel pathways that either exacerbate or mitigate neuronal death. Finally, discuss insights open new avenues for neuroprotective strategies, including chelation inhibitors. By questions, this seeks clarify state knowledge proposes directions harness modulation intervention.

Language: Английский

Ferroptosis and Iron Homeostasis: Molecular Mechanisms and Neurodegenerative Disease Implications DOI Creative Commons
Nurzhan Abdukarimov, Kamilya Kokabi, Jeannette Kunz

et al.

Antioxidants, Journal Year: 2025, Volume and Issue: 14(5), P. 527 - 527

Published: April 28, 2025

Iron dysregulation has emerged as a pivotal factor in neurodegenerative pathologies, especially through its capacity to promote ferroptosis, unique form of regulated cell death driven by iron-catalyzed lipid peroxidation. This review synthesizes current evidence on the molecular underpinnings focusing how disruptions iron homeostasis interact with key antioxidant defenses, such system Xc−-glutathione-GPX4 axis, tip neurons toward lethal oxidative damage. Building these mechanistic foundations, we explore ferroptosis intersects hallmark pathologies Alzheimer’s disease (AD) and Parkinson’s (PD) examine accumulation vulnerable brain regions may fuel disease-specific protein aggregation neurodegeneration. We further surveyed distinct components highlighting role peroxidation enzymes, mitochondrial dysfunction, recently discovered parallel pathways that either exacerbate or mitigate neuronal death. Finally, discuss insights open new avenues for neuroprotective strategies, including chelation inhibitors. By questions, this seeks clarify state knowledge proposes directions harness modulation intervention.

Language: Английский

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