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The Mitochondrial Permeability Transition: Nexus of Aging, Disease and Longevity
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Mitochondrial Cyclosporine A-Independent Palmitate/Ca2+-Induced Permeability Transition Pore (PA-mPT Pore) and Its Role in Mitochondrial Function and Protection against Calcium Overload and Glutamate Toxicity

1
Institute of Theoretical and Experimental Biophysics, RAS, Pushchino, 142290 Moscow, Russia
2
Department of Molecular Pathobiology, College of Dentistry, New York University, New York, NY 10010, USA
*
Author to whom correspondence should be addressed.
Cells 2021, 10(1), 125; https://doi.org/10.3390/cells10010125
Received: 9 December 2020 / Revised: 29 December 2020 / Accepted: 30 December 2020 / Published: 11 January 2021
(This article belongs to the Special Issue Mitochondrial Permeability Transition)
A sharp increase in the permeability of the mitochondrial inner membrane known as mitochondrial permeability transition (or mPT) occurs in mitochondria under the conditions of Ca2+ and ROS stress. Permeability transition can proceed through several mechanisms. The most common mechanism of mPT is based on the opening of a cyclosporine A (CSA)-sensitive protein channel in the inner membrane. In addition to the CSA-sensitive pathway, mPT can occur through the transient opening of lipid pores, emerging in the process of formation of palmitate/Ca2+ complexes. This pathway is independent of CSA and likely plays a protective role against Ca2+ and ROS toxicity. The review considers molecular mechanisms of formation and regulation of the palmitate/Ca2+-induced pores, which we designate as PA-mPT to distinguish it from the classical CSA-sensitive mPT. In the paper, we discuss conditions of its opening in the biological membranes, as well as its role in the physiological and pathophysiological processes. Additionally, we summarize data that indicate the involvement of PA-mPT in the protection of mitochondria against calcium overload and glutamate-induced degradation in neurons. View Full-Text
Keywords: mitochondria; palmitic acid; palmitate/Ca2+-induced permeability transition pore; calcium overload; glutamate toxicity mitochondria; palmitic acid; palmitate/Ca2+-induced permeability transition pore; calcium overload; glutamate toxicity
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MDPI and ACS Style

Mironova, G.D.; Pavlov, E.V. Mitochondrial Cyclosporine A-Independent Palmitate/Ca2+-Induced Permeability Transition Pore (PA-mPT Pore) and Its Role in Mitochondrial Function and Protection against Calcium Overload and Glutamate Toxicity. Cells 2021, 10, 125. https://doi.org/10.3390/cells10010125

AMA Style

Mironova GD, Pavlov EV. Mitochondrial Cyclosporine A-Independent Palmitate/Ca2+-Induced Permeability Transition Pore (PA-mPT Pore) and Its Role in Mitochondrial Function and Protection against Calcium Overload and Glutamate Toxicity. Cells. 2021; 10(1):125. https://doi.org/10.3390/cells10010125

Chicago/Turabian Style

Mironova, Galina D.; Pavlov, Evgeny V. 2021. "Mitochondrial Cyclosporine A-Independent Palmitate/Ca2+-Induced Permeability Transition Pore (PA-mPT Pore) and Its Role in Mitochondrial Function and Protection against Calcium Overload and Glutamate Toxicity" Cells 10, no. 1: 125. https://doi.org/10.3390/cells10010125

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