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Nitric Oxide and Mitochondrial Function in Neurological Diseases.

Mehdi Ghasemi1, Yunis Mayasi2, Anas Hannoun1

  • 1Department of Neurology, University of Massachusetts Medical School, Worcester, MA 01655, USA.

Neuroscience
|February 21, 2018
PubMed
Summary

Nitric oxide (NO) and reactive NO species (RNS) impact mitochondrial function, affecting cellular metabolism and neuronal survival. Understanding these mechanisms is key for neurodegenerative disease treatment.

Keywords:
mitochondriamitochondrial fragmentationneurologic diseasesnitric oxideparthanatosperoxynitrite

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Area of Science:

  • Cellular Biology
  • Neuroscience
  • Biochemistry

Background:

  • Mitochondria are vital organelles for cellular energy production and metabolism.
  • Nitric oxide (NO) is a key signaling molecule that influences mitochondrial activity.
  • Dysfunctional mitochondria are implicated in neurodegenerative diseases.

Purpose of the Study:

  • To review the mechanisms by which excess nitric oxide (NO) and reactive NO species (RNS) impair mitochondrial function.
  • To explore the role of NO-mediated mitochondrial dysfunction in neurodegenerative disease pathogenesis.
  • To highlight potential therapeutic insights for neurodegenerative diseases based on NO signaling pathways.

Main Methods:

  • Review of existing literature on nitric oxide (NO), reactive NO species (RNS), and mitochondrial biology.
  • Analysis of molecular mechanisms linking NO/RNS to mitochondrial dysfunction.
  • Examination of NO's impact on the electron transport chain, mitochondrial permeability, and protein S-nitrosylation.

Main Results:

  • Excess NO/RNS negatively affects the electron transport chain and mitochondrial permeability transition.
  • NO-mediated S-nitrosylation of proteins like DRP-1 and PINK1/Parkin disrupts mitochondrial dynamics and autophagy.
  • NO/RNS alter key metabolic pathways and can induce nuclear toxicity, leading to neuronal cell death via apoptosis-inducing factor (AIF) release.

Conclusions:

  • Nitric oxide (NO) and reactive NO species (RNS) exert multifaceted detrimental effects on mitochondrial function.
  • These NO-mediated mitochondrial impairments contribute significantly to the development of neurodegenerative diseases.
  • Targeting NO signaling pathways in mitochondria offers promising therapeutic strategies for neurodegenerative disorders.