About: Physiopathology of the Permeability Transition Pore: Molecular Mechanisms in Human Pathology

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An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Physiopathology of the Permeability Transition Pore: Molecular Mechanisms in Human Pathology
Creator	Pinton, Paolo Bonora, Massimo Bouhamida, Esmaa Giorgi, Carlotta Kahsay, Asrat Morciano, Giampaolo Patergnani, Simone Pedriali, Gaia Ramaccini, Daniela Wieckowski, Mariusz
source	PMC
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 Ca(2+), 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.
has issue date	2020-07-04(xsd:dateTime)
bibo:doi	10.3390/biom10070998
bibo:pmid	32635556
has license	cc-by
sha1sum (hex)	3f6926262c4fb822216543068582b24e8466feaf
schema:url	https://doi.org/10.3390/biom10070998
resource representing a document's title	Physiopathology of the Permeability Transition Pore: Molecular Mechanisms in Human Pathology
has PubMed Central identifier	PMC7408088
has PubMed identifier	32635556
schema:publication	Biomolecules
resource representing a document's body	covid:3f6926262c4fb822216543068582b24e8466feaf#body_text
is schema:about of	named entity 'MPT' named entity 'events' named entity 'sudden' named entity 'MITOCHONDRIAL PERMEABILITY TRANSITION' named entity 'HERE' named entity 'MPT' named entity 'mitochondrial membrane' named entity 'loss' named entity 'activation' named entity 'dependent' named entity 'etiology' named entity 'molecular-weight' named entity 'MPT' named entity 'Mitochondrial permeability transition' named entity 'MPT' named entity 'metabolic' named entity 'biomolecules' named entity 'Human Pathology' named entity 'kDa' named entity 'demyelination' named entity 'muscle diseases' named entity 'mitochondrial matrix' named entity 'cytoskeleton' named entity 'inflammatory response' named entity 'degenerative diseases' named entity 'risk factors' named entity 'Bcl-2' named entity 'carboxyatractyloside' named entity 'Bak' named entity 'phosphorylates' named entity 'membrane permeabilization' named entity 'quality control' named entity 'hydrogen ions' named entity 'Ppif' named entity 'ADP/ATP translocase' named entity 'apoptosis' named entity 'chronic liver' named entity 'PINK1' named entity 'myofibril' named entity 'Bax' named entity 'ATP' named entity 'SERCA' named entity 'CsA' named entity 'ATP synthase' named entity 'NAFLD' named entity 'ADP' named entity 'ATP synthase' named entity 'apoptosome' named entity 'MPT' named entity 'Bcl-xL' named entity 'mitochondrial' named entity 'substrate' named entity 'cytochrome' named entity 'zebrafish' named entity 'human diseases' named entity 'MERRF' named entity 'ischemia' named entity 'mitochondrial respiration' named entity 'lipid peroxidation' named entity 'pathogenesis' named entity 'neurons' named entity 'PTP' named entity 'procaspases' named entity 'OMM' named entity 'necrosis' named entity 'ROS' named entity 'ATP' named entity 'cyclosporine' named entity 'KO mice' named entity 'mitochondrial' named entity 'transgenic' named entity 'ATP synthesis'

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