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Assessment of Open Probability of the Mitochondrial Permeability Transition Pore in the Setting of Coenzyme Q Excess
Published on: June 1, 2022
Mitochondrial calcium and the permeability transition in cell death
John J Lemasters1, Tom P Theruvath, Zhi Zhong
1Center for Cell Death, Injury and Regeneration, Medical University of South Carolina, Charleston, SC 29425, USA. JJLemasters@musc.edu
Biochimica Et Biophysica Acta
|July 7, 2009
Summary
Calcium (Ca2+) dysregulation contributes to cell injury via mitochondrial permeability transition (MPT). The role of Ca2+ in MPT induction varies depending on the specific biological context and cell type.
Area of Science:
- Cellular Biology
- Biochemistry
- Pathology
Background:
- Calcium (Ca2+) dysregulation is a known factor in cellular injury.
- The mitochondrial permeability transition (MPT) is a Ca2+-linked process implicated in necrosis and apoptosis.
Purpose of the Study:
- To elucidate the multifaceted role of calcium (Ca2+) in the induction of mitochondrial permeability transition (MPT) across various cellular injury models.
Main Methods:
- Review and synthesis of existing literature on Ca2+ and MPT.
- Analysis of different biological settings including ischemia-reperfusion, Reye-related agents, and oxidative stress.
Main Results:
- Ca2+ overload can directly induce MPT.
- In cardiac myocytes post-ischemia-reperfusion, Ca2+ overload is a consequence, not a cause, of MPT.
- Ca2+ acts permissively in Reye-related agent cytotoxicity and liver graft storage-reperfusion injury.
- Mitochondrial Ca2+ and reactive oxygen species (ROS) synergize to induce MPT in oxidative stress.
Conclusions:
- The specific role of Ca2+ in triggering MPT and subsequent cell death is highly context-dependent.
- Understanding these varying roles is crucial for developing targeted therapeutic strategies against cell injury.
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