Physiopathology of the Permeability Transition Pore: Molecular Mechanisms in Human Pathology
Year: 2020
Type: review
Abstract: Mitochondrial permeability transition (MPT) is the sudden loss in the permeability of the inner mitochondrial membrane (IMM) to low-molecular-weight solutes. Due to osmotic forces, MPT is paralleled by a massive influx of water into the mitochondrial matrix, eventually leading to the structural collapse of the organelle. Thus, MPT can initiate outer-mitochondrial-membrane permeabilization (MOMP), promoting the activation of the apoptotic caspase cascade and caspase-independent cell-death mechanisms. The induction of MPT is mostly dependent on mitochondrial reactive oxygen species (ROS) and Ca2+, but is also dependent on the metabolic stage of the affected cell and signaling events. Therefore, since its discovery in the late 1970s, the role of MPT in human pathology has been heavily investigated. Here, we summarize the most significant findings corroborating a role for MPT in the etiology of a spectrum of human diseases, including diseases characterized by acute or chronic loss of adult cells and those characterized by neoplastic initiation.
Source: Biomolecules
DOI: 10.3390/biom10070998
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $1,901
Awards: G1022401633, G1609110573, G1746732529, G2781501609, G312915963, G4067818967, G4302731059, G434337789, G4655939736, Promyelocytic leukemia protein (PML) outside the tumor: a new player in the control of inflammation, G5647888045, G5696865441, G5835068126, Bioenergetic Remodeling in the Pathophysiology and Treatment of Non-Alcoholic Fatty Liver Disease, G8962454259, mitoFOIE GRAS: Non-invasive Profiling of Mitochondrial Function in Non-Alcoholic Fatty Liver Disease
OpenAlex ID: W3038384160