Redox-based endoplasmic reticulum dysfunction in neurological diseases

Research output: Contribution to journalArticle

32 Citations (Scopus)

Abstract

The redox homeostasis of the endoplasmic reticulum lumen is characteristically different from that of the other subcellular compartments. The concerted action of membrane transport processes and oxidoreductase enzymes maintain the oxidized state of the thiol-disulfide and the reducing state of the pyridine nucleotide redox systems, which are prerequisites for the normal functions of the organelle. The powerful thiol-oxidizing machinery allows oxidative protein folding but continuously challenges the local antioxidant defense. Alterations of the cellular redox environment either in oxidizing or reducing direction affect protein processing and may induce endoplasmic reticulum stress and unfolded protein response. The activated signaling pathways attempt to restore the balance between protein loading and processing and induce apoptosis if the attempt fails. Recent findings strongly support the involvement of this mechanism in brain ischemia, neuronal degenerative diseases and traumatic injury. The redox changes in the endoplasmic reticulum are integral parts of the pathomechanism of neurological diseases, either as causative agents, or as complications.

Original languageEnglish
Pages (from-to)20-34
Number of pages15
JournalJournal of Neurochemistry
Volume107
Issue number1
DOIs
Publication statusPublished - Oct 2008

Fingerprint

Endoplasmic Reticulum
Oxidation-Reduction
Sulfhydryl Compounds
Protein folding
Unfolded Protein Response
Proteins
Endoplasmic Reticulum Stress
Protein Folding
Processing
Heat-Shock Proteins
Brain Ischemia
Disulfides
Organelles
Machinery
Brain
Oxidoreductases
Homeostasis
Nucleotides
Antioxidants
Apoptosis

Keywords

  • Apoptosis
  • Endoplasmic reticulum stress
  • Neuron
  • Oxidative stress
  • Unfolded protein response

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

Cite this

Redox-based endoplasmic reticulum dysfunction in neurological diseases. / Bánhegyi, G.; Mandl, J.; Csala, M.

In: Journal of Neurochemistry, Vol. 107, No. 1, 10.2008, p. 20-34.

Research output: Contribution to journalArticle

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