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dc.contributor.authorPérez M.J.
dc.contributor.authorQuintanilla R.A.
dc.date.accessioned2020-09-02T22:26:20Z
dc.date.available2020-09-02T22:26:20Z
dc.date.issued2017
dc.identifier10.1016/j.ydbio.2017.04.018
dc.identifier.citation426, 1, 1-7
dc.identifier.issn00121606
dc.identifier.urihttps://hdl.handle.net/20.500.12728/5870
dc.descriptionMitochondria is not only a dynamic organelle that produces ATP, but is also an important contributor to cell functions in both development and cell death processes. These paradoxical functions of mitochondria are partially regulated by the mitochondrial permeability transition pore (mPTP), a high-conductance channel that can induce loss of mitochondrial membrane potential, impairment of cellular calcium homeostasis, oxidative stress, and a decrease in ATP production upon pathological activation. Interestingly, despite their different etiologies, several neurodegenerative diseases and heart ischemic injuries share mitochondrial dysfunction as a common element. Generally, mitochondrial impairment is triggered by calcium deregulation that could lead to mPTP opening and cell death. Several studies have shown that opening of the mPTP not only induces mitochondrial damage and cell death, but is also a physiological mechanism involved in different cellular functions. The mPTP participates in regular calcium-release mechanisms that are required for proper metabolic regulation; it is hypothesized that the transient opening of this structure could be the principal mediator of cardiac and brain development. The mPTP also plays a role in protecting against different brain and cardiac disorders in the elderly population. Therefore, the aim of this work was to discuss different studies that show this controversial characteristic of the mPTP; although mPTP is normally associated with several pathological events, new critical findings suggest its importance in mitochondrial function and cell development. © 2017 Elsevier Inc.
dc.language.isoen
dc.publisherAcademic Press Inc.
dc.subjectCalcium
dc.subjectCardiac development
dc.subjectMitochondria
dc.subjectMitochondrial permeability transition pore
dc.subjectNeuronal development
dc.subjectOxidative stress
dc.subjectmitochondrial permeability transition pore
dc.subjectadenosine triphosphate
dc.subjectcalcium
dc.subjectcarrier protein
dc.subjectmitochondrial permeability transition pore
dc.subjectAlzheimer disease
dc.subjectexcitotoxicity
dc.subjectheart development
dc.subjectheart muscle ischemia
dc.subjectHuntington chorea
dc.subjectnervous system development
dc.subjectnonhuman
dc.subjectParkinson disease
dc.subjectpriority journal
dc.subjectprotein function
dc.subjectReview
dc.subjectanimal
dc.subjectbiosynthesis
dc.subjectcardiac muscle cell
dc.subjectcardiomyopathy
dc.subjectcytology
dc.subjectdegenerative disease
dc.subjectembryology
dc.subjectgrowth, development and aging
dc.subjectheart
dc.subjecthuman
dc.subjectmetabolism
dc.subjectmitochondrial membrane potential
dc.subjectmitochondrion
dc.subjectmouse
dc.subjectoxidative stress
dc.subjectpathology
dc.subjectphysiology
dc.subjectAdenosine Triphosphate
dc.subjectAnimals
dc.subjectCalcium
dc.subjectCardiomyopathies
dc.subjectHeart
dc.subjectHumans
dc.subjectMembrane Potential, Mitochondrial
dc.subjectMice
dc.subjectMitochondria
dc.subjectMitochondrial Membrane Transport Proteins
dc.subjectMyocytes, Cardiac
dc.subjectNeurodegenerative Diseases
dc.subjectOxidative Stress
dc.titleDevelopment or disease: duality of the mitochondrial permeability transition pore
dc.typeReview


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