Pathophysiologic role of ischemia reperfusion injury: A review

Vishwakarma, Vishal Kumar; Upadhyay, Prabhat Kumar; Gupta, Jeetendra Kumar; Yadav, Harlokesh Narayan

doi:10.1016/j.jicc.2017.06.017

Cited by 13 publications

(8 citation statements)

References 80 publications

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“…Multiple pairwise comparisons ( Supplementary Table S4 ) showed that most of these significant variations in relative lipid abundance occurred between CT versus IR (128 species), followed by CT versus ISC and IR versus ISC (80 species each). This suggests that reperfusion induced more profound changes than ISC, which is consistent with previous reports suggesting that the injury usually associated with ischemia is intensified during reperfusion [ 17 , [65] , [66] , [67] , [68] ].…”

Section: Discussionsupporting

confidence: 91%

“…PC, but also PE, are the main components of cell membranes, and changes in structural phospholipids have been associated with changes in membrane properties. These include Ca 2+ imbalance and changes in the permeability of the myocardial membrane [ 67 , 83 ], which can lead to cell death by destabilisation of the membrane. Phospholipid metabolism is affected during myocardial ischemia, and most studies reporting modulation of the PL profile attribute these changes to oxidised phospholipids [ 78 , 80 ] and their degradation by phospholipase A2 (PLA2) with the formation of bioactive eicosanoids and lysoPLs, which are important inflammatory mediators [ 72 , 73 , 84 ].…”

Section: Discussionmentioning

confidence: 99%

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Cardiac phospholipidome is altered during ischemia and reperfusion in an ex vivo rat model

Montero-Bullón

Aveiro

Melo

et al. 2021

Biochemistry and Biophysics Reports

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Acute myocardial infarction (AMI) is the leading cause of death, morbidity, and health costs worldwide. In AMI, a sudden blockage of blood flow causes myocardial ischemia and cell death. Reperfusion after ischemia has paradoxical effects and may exacerbate the myocardial injury, a process known as ischemic reperfusion injury. In this work we evaluated the lipidome of isolated rat hearts, maintained in controlled perfusion (CT), undergoing global ischemia (ISC) or ischemia followed by reperfusion (IR). 153 polar lipid levels were significantly different between conditions. 48 features had q < 0.001 and included 8 phosphatidylcholines and 4 lysophospholipids, which were lower in ISC compared to CT, and even lower in the IR group, suggesting that IR induces more profound changes than ISC. We observed that the levels of 16 alkyl acyl phospholipids were significantly altered during ISC and IR. Overall, these data indicate that myocardial lipid remodelling and possibly damage occurs to a greater extent during reperfusion. The adaptation of cardiac lipidome during ISC and IR described is consistent with the presence of oxidative damage and may reflect the impact of AMI on the lipidome at the cellular level and provide new insights into the role of lipids in the pathophysiology of acute myocardial ischemia/reperfusion injury.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Cardiac phospholipidome is altered during ischemia and reperfusion in an ex vivo rat model

Montero-Bullón

Aveiro

Melo

et al. 2021

Biochemistry and Biophysics Reports

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“…During ischemia, a large increase in the antioxidant defense system, such as glutathione augmentation, has been seen in an attempt to deal with oxidative stress [ 156 , 157 ]. Moreover, N-acetylcysteine, angiotensin-converting enzyme inhibitors, catalase, mannitol, superoxide dismutase, and vitamin E have been shown to have antioxidant properties that help to prevent I-R injury [ 158 ].…”

Section: Role Of Oxidative Stress In the Generation Of Cardiovascular Diseasesmentioning

confidence: 99%

Glutathione Participation in the Prevention of Cardiovascular Diseases

et al. 2021

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Cardiovascular diseases (CVD) (such as occlusion of the coronary arteries, hypertensive heart diseases and strokes) are diseases that generate thousands of patients with a high mortality rate worldwide. Many of these cardiovascular pathologies, during their development, generate a state of oxidative stress that leads to a deterioration in the patient’s conditions associated with the generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS). Within these reactive species we find superoxide anion (O2•–), hydroxyl radical (•OH), nitric oxide (NO•), as well as other species of non-free radicals such as hydrogen peroxide (H2O2), hypochlorous acid (HClO) and peroxynitrite (ONOO–). A molecule that actively participates in counteracting the oxidizing effect of reactive species is reduced glutathione (GSH), a tripeptide that is present in all tissues and that its synthesis and/or regeneration is very important to be able to respond to the increase in oxidizing agents. In this review, we will address the role of glutathione, its synthesis in both the heart and the liver, and its importance in preventing or reducing deleterious ROS effects in cardiovascular diseases.

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“…In the endothelial tissue, the production of cytokines increases with bioactive substances such as endothelin and thromboxane. Thereby, tissues will become more vulnerable to reperfusion 9 . The pathophysiological mechanism of myocardial I/R is shown in Figure 1.…”

Section: Pathophysiological Mechanism Of I/r Injurymentioning

confidence: 99%

“…Reperfusion of ischaemic myocardial tissue results in reversible and contraction dysfunction. Although restoration of blood flow to an ischaemic organ prevents irreversible cellular injury, reperfusion alone causes more tissue damage than is caused by ischaemia 9 …”

Section: Introductionmentioning

confidence: 99%

A review of myocardial ischaemia/reperfusion injury: Pathophysiology, experimental models, biomarkers, genetics and pharmacological treatment

Gunata

Parlakpınar

2020

Cell Biochemistry & Function

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Cardiovascular diseases are known to be the most fatal diseases worldwide. Ischaemia/reperfusion (I/R) injury is at the centre of the pathology of the most common cardiovascular diseases. According to the World Health Organization estimates, ischaemic heart disease is the leading global cause of death, causing more than 9 million deaths in 2016. After cardiovascular events, thrombolysis, percutaneous transluminal coronary angioplasty or coronary bypass surgery are applied as treatment. However, after restoring coronary blood flow, myocardial I/R injury may occur. It is known that this damage occurs due to many pathophysiological mechanisms, especially increasing reactive oxygen types. Besides causing cardiomyocyte death through multiple mechanisms, it may be an important reason for affecting other cell types such as platelets, fibroblasts, endothelial and smooth muscle cells and immune cells. Also, polymorphonuclear leukocytes are associated with myocardial I/R damage during reperfusion. This damage may be insufficient in patients with co‐morbidity, as it is demonstrated that it can be prevented by various endogenous antioxidant systems. In this context, the resulting data suggest that optimal cardioprotection may require a combination of additional or synergistic multi‐target treatments. In this review, we discussed the pathophysiology, experimental models, biomarkers, treatment and its relationship with genetics in myocardial I/R injury. Significance of the study This review summarized current information on myocardial ischaemia/reperfusion injury (pathophysiology, experimental models, biomarkers, genetics and pharmacological therapy) for researchers and reveals guiding data for researchers, especially in the field of cardiovascular system and pharmacology.

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Pathophysiologic role of ischemia reperfusion injury: A review

Cited by 13 publications

References 80 publications

Cardiac phospholipidome is altered during ischemia and reperfusion in an ex vivo rat model

Cardiac phospholipidome is altered during ischemia and reperfusion in an ex vivo rat model

Glutathione Participation in the Prevention of Cardiovascular Diseases

A review of myocardial ischaemia/reperfusion injury: Pathophysiology, experimental models, biomarkers, genetics and pharmacological treatment

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