Therapeutics for Ferroptosis in CNS Disease

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: 20 June 2024 | Viewed by 263

Special Issue Editor

Institute for Research in Physiopathology and Clinical Biochemistry (INFIBIOC), Clinical Biochemistry Department, School of Pharmacy and Biochemistry (FFyB), University of Buenos Aires, Buenos Aires, Argentina
Interests: ABC-transporters; refractory epilepsy; hypoxia; pharmacoresistance

Special Issue Information

Dear Colleagues,

Iron (Fe) is a vital element in oxygen transport, enzyme activity, and oxide-reduction reactions for almost all organisms. However, iron is responsible for a recently described programmed cell death mechanism, characterized by the intracellular accumulation of iron and high production of reactive oxygen species. This process is known as ferroptosis, where antioxidant defenses such as glutathione peroxidase 4 (GPX4) are inhibited or overwhelmed. For proper intracellular use, iron must cross biological membranes, which requires conversion from its oxidized to reduced state and vice versa, depending on the metabolic step involved. These oxidation-reduction state exchanges can be unbalanced as a consequence of a long list of pathological processes that lead to an inadequate accumulation of intracellular Fe, which is prone to favoring the generation of free radicals and inducing cell damage/death caused by lipid peroxidation. The complex molecular mechanisms involved in ferroptosis can be activated in all cell types, including those of the CNS, developing degenerative (NDG) processes also known as neurodegeneration. The progressive loss of neural functions and neuronal death with iron accumulation is closely associated with intellectual and/or motor impairment as observed in several diseases that mainly affect older people such as Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), Parkinson’s disease (PD), stroke, Huntington’s disease, Creutzfeldt‒Jakob disease, multiple sclerosis, and, more recently, also described in Epilepsy. Since the description of this particular pattern of iron-dependent cell death called ferroptosis by Dixon et al. in 2012, a wide range of evidence has suggested that ferroptosis is a potential therapeutic target to prevent, protect, or at least alleviate the development of the acquired NDG process or the genetically encoded Neurodegeneration with Brain Iron Accumulation (NBIA) diseases. In this Special Issue of Pharmaceuticals, we intend to update the most relevant information on the potential therapeutic action of ferroptosis in the CNS, with a focus on its implication in different types of neurological pathologies and its most representative biomarkers.

Prof. Dr. Alberto Lazarowski
Guest Editor

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Keywords

  • iron
  • free radicals
  • oxidative stress
  • neurodegeneration
  • hypoxia
  • antioxidants
  • iron chelators
  • ABC transporters

Published Papers

This special issue is now open for submission.
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