Mitochondrial Channels in Neurodegeneration

Pablo M. Peixoto, Kathleen W. Kinnally, Evgeny Pavlov

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

This chapter enables the reader to become acquainted with the currently known mitochondrial channels, some of which have unknown functions and whose study in neurons may inspire potential approaches to treatment of neurodegenerative diseases. Although fine regulation of the channels might vary from organ to organ, it is likely that general properties of these channels will be similar and thus can be applied to neurons. The channels discussed in the chapter include voltage dependent anion-selective channel (VDAC), protein import channels, mitochondrial Ca2+ channels, Mrs2 - Mg2+ channel. The mitochondrial channels with established roles in neuronal death include mitochondrial apoptosis-induced channel (MAC) and VDAC of the outer membrane and the mitochondrial permeability transition pore (mPTP) of the inner membrane. There is also an increasing interest in the role of mitochondrial ATP-dependent potassium channels (KATP) in neuronal degeneration, especially because of their established role in hypoxic preconditioning in the heart.

Original languageEnglish (US)
Title of host publicationThe Functions, Disease-Related Dysfunctions, and Therapeutic Targeting of Neuronal Mitochondria
PublisherWiley
Pages65-100
Number of pages36
ISBN (Electronic)9781119017127
ISBN (Print)9781118709238
DOIs
StatePublished - Sep 25 2015

Keywords

  • Dying cell
  • Healthy neuron
  • KATP
  • MAC
  • Mitochondrial channels
  • Mrs2 - Mg channels
  • Neurodegenerative diseases
  • Protein import channels
  • VDAC

ASJC Scopus subject areas

  • Chemistry(all)
  • Medicine(all)
  • Neuroscience(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)

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  • Cite this

    Peixoto, P. M., Kinnally, K. W., & Pavlov, E. (2015). Mitochondrial Channels in Neurodegeneration. In The Functions, Disease-Related Dysfunctions, and Therapeutic Targeting of Neuronal Mitochondria (pp. 65-100). Wiley. https://doi.org/10.1002/9781119017127.ch3