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Updated: Jul 4, 2026

Assessment of Open Probability of the Mitochondrial Permeability Transition Pore in the Setting of Coenzyme Q Excess
07:35

Assessment of Open Probability of the Mitochondrial Permeability Transition Pore in the Setting of Coenzyme Q Excess

Published on: June 1, 2022

Identification of thioredoxin-2 as a regulator of the mitochondrial permeability transition

Min He1, Jiyang Cai, Young-Mi Go

  • 1Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, Emory University, Atlanta, GA 30322, USA.

Toxicological Sciences : an Official Journal of the Society of Toxicology
|June 14, 2008
PubMed

Insights

Thioredoxin-2 (Trx2) protein protects mitochondria from cell death. This study shows Trx2 prevents mitochondrial permeability transition (MPT) triggered by oxidants and calcium, highlighting its role in regulating cell death.

Area of Science:

  • Mitochondrial biology
  • Cell death mechanisms
  • Oxidative stress

Background:

  • Thioredoxin-2 (Trx2) is a mitochondria-specific protein that inhibits cell death.
  • Mitochondrial permeability transition (MPT) is a key cell death pathway activated by oxidants and associated with necrosis and apoptosis.

Purpose of the Study:

  • To investigate the protective role of Trx2 against oxidant-induced MPT.
  • To determine if Trx2 regulates MPT independently of oxidative stress.

Main Methods:

  • Experiments were conducted using isolated mitochondria from Trx2 transgenic mice.
  • MPT was induced by exogenously added peroxide and calcium ions (Ca2+).

Main Results:

  • Trx2 demonstrated protection against MPT induced by peroxide.
  • Unexpectedly, Trx2 also inhibited MPT induced by Ca2+ alone, without added peroxide.

Conclusions:

  • Trx2 not only protects against oxidative stress but also acts as an endogenous regulator of MPT.
  • These findings suggest Trx2 has a broader role in controlling mitochondrial cell death pathways.

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