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Oxidative Stress and Lung Ischemia-Reperfusion Injury.

Ferrari RS, Andrade CF - Oxid Med Cell Longev (2015)

Bottom Line: Several studies have confirmed the destructiveness of the toxic oxygen metabolites produced and their role in the pathophysiology of different processes, such as oxygen poisoning, inflammation, and ischemic injury.Due to the different degrees of tissue damage resulting from the process of ischemia and subsequent reperfusion, several studies in animal models have focused on the prevention of IR injury and methods of lung protection.Lung IR injury has clinical relevance in the setting of lung transplantation and cardiopulmonary bypass, for which the consequences of IR injury may be devastating in critically ill patients.

View Article: PubMed Central - PubMed

Affiliation: Thoracic Surgery Department, Laboratory of Airways and Lung, Hospital of Clínicas of Porto Alegre, Ramiro Barcelos 2.350, 90035-903 Porto Alegre, RS, Brazil ; Federal University of Rio Grande of Sul (FRGS), Rua Ramiro Barcelos 2400, 2° andar Bairro Santana, 90035-003 Porto Alegre, RS, Brazil.

ABSTRACT
Ischemia-reperfusion (IR) injury is directly related to the formation of reactive oxygen species (ROS), endothelial cell injury, increased vascular permeability, and the activation of neutrophils and platelets, cytokines, and the complement system. Several studies have confirmed the destructiveness of the toxic oxygen metabolites produced and their role in the pathophysiology of different processes, such as oxygen poisoning, inflammation, and ischemic injury. Due to the different degrees of tissue damage resulting from the process of ischemia and subsequent reperfusion, several studies in animal models have focused on the prevention of IR injury and methods of lung protection. Lung IR injury has clinical relevance in the setting of lung transplantation and cardiopulmonary bypass, for which the consequences of IR injury may be devastating in critically ill patients.

No MeSH data available.


Related in: MedlinePlus

Release of cytochrome C from mitochondria triggers the activation of caspase 9, which cleaves caspases 3 and 6, leading to apoptosis.
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Related In: Results  -  Collection


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fig4: Release of cytochrome C from mitochondria triggers the activation of caspase 9, which cleaves caspases 3 and 6, leading to apoptosis.

Mentions: An important regulator of apoptosis following DNA damage is p53, which can induce Bax and Bak, regulating the release of cytochrome C from mitochondria and thereby initiating the cascade leading to apoptosis [110]. Cytochrome C binds to apoptotic protease activating factor 1 (Apaf-1), activating caspase 9, which in turn cleaves caspases 3 and 6 [111, 112], leading to cell death (Figure 4).


Oxidative Stress and Lung Ischemia-Reperfusion Injury.

Ferrari RS, Andrade CF - Oxid Med Cell Longev (2015)

Release of cytochrome C from mitochondria triggers the activation of caspase 9, which cleaves caspases 3 and 6, leading to apoptosis.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4487720&req=5

fig4: Release of cytochrome C from mitochondria triggers the activation of caspase 9, which cleaves caspases 3 and 6, leading to apoptosis.
Mentions: An important regulator of apoptosis following DNA damage is p53, which can induce Bax and Bak, regulating the release of cytochrome C from mitochondria and thereby initiating the cascade leading to apoptosis [110]. Cytochrome C binds to apoptotic protease activating factor 1 (Apaf-1), activating caspase 9, which in turn cleaves caspases 3 and 6 [111, 112], leading to cell death (Figure 4).

Bottom Line: Several studies have confirmed the destructiveness of the toxic oxygen metabolites produced and their role in the pathophysiology of different processes, such as oxygen poisoning, inflammation, and ischemic injury.Due to the different degrees of tissue damage resulting from the process of ischemia and subsequent reperfusion, several studies in animal models have focused on the prevention of IR injury and methods of lung protection.Lung IR injury has clinical relevance in the setting of lung transplantation and cardiopulmonary bypass, for which the consequences of IR injury may be devastating in critically ill patients.

View Article: PubMed Central - PubMed

Affiliation: Thoracic Surgery Department, Laboratory of Airways and Lung, Hospital of Clínicas of Porto Alegre, Ramiro Barcelos 2.350, 90035-903 Porto Alegre, RS, Brazil ; Federal University of Rio Grande of Sul (FRGS), Rua Ramiro Barcelos 2400, 2° andar Bairro Santana, 90035-003 Porto Alegre, RS, Brazil.

ABSTRACT
Ischemia-reperfusion (IR) injury is directly related to the formation of reactive oxygen species (ROS), endothelial cell injury, increased vascular permeability, and the activation of neutrophils and platelets, cytokines, and the complement system. Several studies have confirmed the destructiveness of the toxic oxygen metabolites produced and their role in the pathophysiology of different processes, such as oxygen poisoning, inflammation, and ischemic injury. Due to the different degrees of tissue damage resulting from the process of ischemia and subsequent reperfusion, several studies in animal models have focused on the prevention of IR injury and methods of lung protection. Lung IR injury has clinical relevance in the setting of lung transplantation and cardiopulmonary bypass, for which the consequences of IR injury may be devastating in critically ill patients.

No MeSH data available.


Related in: MedlinePlus