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Cellular and molecular mechanisms of cell damage and cell death in ischemia–reperfusion injury in organ transplantation

Dugbartey, George J.

Molecular biology reports, 2024-12, Vol.51 (1), p.473, Article 473 [Periódico revisado por pares]

Dordrecht: Springer Netherlands

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Título:
Cellular and molecular mechanisms of cell damage and cell death in ischemia–reperfusion injury in organ transplantation
Autor: Dugbartey, George J.
Assuntos: Animal Anatomy ; Animal Biochemistry ; Apoptosis ; Autophagy ; Bioenergetics ; Biomedical and Life Sciences ; Cell activation ; Cell Death ; Cell survival ; Edema ; Electron transport chain ; Ferroptosis ; Histology ; Humans ; Hypoxia ; Inflammation ; Ischemia ; Life Sciences ; Metabolism ; Mitophagy ; Molecular modelling ; Morphology ; Necroptosis ; Necrosis ; Organ Transplantation - adverse effects ; Permeability ; Pyroptosis ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Reperfusion ; Reperfusion Injury - metabolism ; Review ; Transplantation ; Transplants & implants
É parte de: Molecular biology reports, 2024-12, Vol.51 (1), p.473, Article 473
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
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Descrição: Ischemia–reperfusion injury (IRI) is a critical pathological condition in which cell death plays a major contributory role, and negatively impacts post-transplant outcomes. At the cellular level, hypoxia due to ischemia disturbs cellular metabolism and decreases cellular bioenergetics through dysfunction of mitochondrial electron transport chain, causing a switch from cellular respiration to anaerobic metabolism, and subsequent cascades of events that lead to increased intracellular concentrations of Na + , H + and Ca 2+ and consequently cellular edema. Restoration of blood supply after ischemia provides oxygen to the ischemic tissue in excess of its requirement, resulting in over-production of reactive oxygen species (ROS), which overwhelms the cells’ antioxidant defence system, and thereby causing oxidative damage in addition to activating pro-inflammatory pathways to cause cell death. Moderate ischemia and reperfusion may result in cell dysfunction, which may not lead to cell death due to activation of recovery systems to control ROS production and to ensure cell survival. However, prolonged and severe ischemia and reperfusion induce cell death by apoptosis, mitoptosis, necrosis, necroptosis, autophagy, mitophagy, mitochondrial permeability transition (MPT)-driven necrosis, ferroptosis, pyroptosis, cuproptosis and parthanoptosis. This review discusses cellular and molecular mechanisms of these various forms of cell death in the context of organ transplantation, and their inhibition, which holds clinical promise in the quest to prevent IRI and improve allograft quality and function for a long-term success of organ transplantation.
Editor: Dordrecht: Springer Netherlands
Idioma: Inglês

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Cellular and molecular mechanisms of cell damage and cell death in ischemia–reperfusion injury in organ transplantation

Dugbartey, George J.

Dordrecht: Springer Netherlands

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