Mitochondrial Permeability Transition: A Look from a Different Angle

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Scopus citations

Abstract

Calcium ions occupy an exceptional niche in cell physiology and biochemistry because of their chemical properties and unique distribution across the plasma membrane. Ca2+ participates in diverse signaling pathways and regulates activity of various intracellular enzymes in neurons. Ca2+ is critical for neuronal survival. Under certain circumstances, excessive Ca2+ accumulation in mitochondria can cause mitochondrial damage manifested in the activation of the mitochondrial permeability transition pore (PTP). This chapter discusses a few selected questions concerning PTP function and structure. The concept of mitochondrial permeability transition (mPT) was formulated by Hunter and Haworth only in the late 1970s, when they used the term Ca2+-induced membrane transition in mitochondria to signify the large increase in inner membrane permeability and the key role of Ca2+ in triggering this phenomenon. They demonstrated that the Ca2+-induced membrane transition in mitochondria leads to mitochondrial uncoupling, release of previously accumulated Ca2+, and mitochondrial swelling.

Original languageEnglish (US)
Title of host publicationThe Functions, Disease-Related Dysfunctions, and Therapeutic Targeting of Neuronal Mitochondria
Publisherwiley
Pages3-30
Number of pages28
ISBN (Electronic)9781119017127
ISBN (Print)9781118709238
DOIs
StatePublished - Sep 25 2015

Keywords

  • Ca2+-induced membrane transition
  • Intracellular calcium
  • Mitochondrial permeability transition
  • Mitochondrial swelling
  • Mitochondrial transition pore
  • Mitochondrial uncoupling
  • Neurons

ASJC Scopus subject areas

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

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  • Cite this

    Broustovetski, N. (2015). Mitochondrial Permeability Transition: A Look from a Different Angle. In The Functions, Disease-Related Dysfunctions, and Therapeutic Targeting of Neuronal Mitochondria (pp. 3-30). wiley. https://doi.org/10.1002/9781119017127.ch1