Mechanistic correlation between mitochondrial permeability transition pores and mitochondrial ATP dependent potassium channels in ischemia reperfusion - 29/04/23
, Ghadeer M. Albadrani c, Ahmed E. Altyar d, e, Mohamed M. Abdel-Daim f, g, Thakur Gurjeet Singh a, ⁎, 1, 2, 3 

Abstract |
Mitochondrial dysfunction is one of the fundamental causes of ischemia reperfusion (I/R) damage. I/R refers to the paradoxical progression of cellular dysfunction and death that occurs when blood flow is restored to previously ischemic tissues. I/R causes a significant rise in mitochondrial permeability resulting in the opening of mitochondrial permeability transition pores (MPTP). The MPTP are broad, nonspecific channels present in the inner mitochondrial membrane (IMM), and are known to mediate the deadly permeability alterations that trigger mitochondrial driven cell death. Protection from reperfusion injury occurs when long-term ischemia is accompanied by short-term ischemic episodes or inhibition of MPTP from opening via mitochondrial ATP dependent potassium (mitoK ATP ) channels. These channels located in the IMM, play an essential role in ischemia preconditioning (PC) and protect against cell death by blocking MPTP opening. This review primarily focuses on the interaction between the MPTP and mitoK ATP along with their role in the I/R injury. This article also describes the molecular composition of the MPTP and mitoK ATP in order to promote future knowledge and treatment of diverse I/R injuries in various organs.
Le texte complet de cet article est disponible en PDF.Abbreviations : I/R, ROS, IMM, MPTP, mitoK ATP , VDAC, PBR, OSCP, PI3-K, GPCRs, PIP3, PDK, ERK, eNOS, PKG, JAK/STAT, RISK
Keywords : Mitochondrial permeability transition pores, Mitochondrial ATP dependent potassium channels, Ischemia reperfusion, Reactive oxygen species, Protein kinase C
Plan
Vol 162
Article 114599- juin 2023 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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