Abstract
If the blood flow slows down and the tissues and organs cannot be delivered the oxygen they need, the lack of sufficient oxygen level is called ischemia, and the restoration of blood flow to tissues and organs is called reperfusion. The damage that occurs after ischemia-reperfusion is called ischemia-reperfusion injury. The complexity of the mechanisms that cause ischemia-reperfusion injury prevents the complete elucidation of this mechanism. Ischemic conditions may lead to irreversible consequences such as cerebral infarction and myocardial infarction. Myocardial ischemia-reperfusion injury is a pathogenic mechanism of heart failure and myocardial infarction and is a major health problem worldwide. Several important pathological processes are involved in ischemia-reperfusion injury, including oxidative stress, programmed cell death (ferroptosis, apoptosis, necrosis), fibrosis, cardiomyocyte hypertrophy, and inflammatory response. Many studies have been conducted to clarify the mechanisms and treatment modalities involved in ischemia-reperfusion injury. This is because ischemia-reperfusion injury is one of the leading causes of death, similar to myocardial infarction, peripheral vascular diseases, etc. Recently, revascularization methods have been used to reduce the level of ischemic damage. In this review, we will briefly discuss the mechanism of cardiac injury and ischemia-reperfusion injury.
Keywords
Limitations
The pathophysiology of IRH is not easily understood because the damage that occurs during the ischemic phase is not well differentiated from the damage that occurs during the reperfusion phase. It is very difficult for clinicians to determine a treatment method that they can use to ameliorate the damage. Therefore, more extensive studies are needed to investigate ischemic disorders, especially myocardial IRH, in more detail.
Conclusion
IRH is the leading cause of death in ischemic disorders.8 As the underlying mechanism of myocardial IRH is complex, complex multi- targeted therapy may be effective in ameliorating reperfusion injury. Therefore, new therapeutic targets should be explored to maximize the benefits of revascularization.23
Declarations
Ethics Declarations
The authors declare that all procedures performed in this study were conducted in accordance with institutional, national, and international ethical standards.
Informed Consent
Not applicable.
Data Availability
No new data were generated or analyzed in this study. Not applicable.
Conflict of Interest
The authors declare that there is no conflict of interest.
Funding
None.
Abbreviations
ACE: Angiotensin-converting enzyme
ATP: Adenosine triphosphate
CABG: Coronary artery bypass grafting
DAMPs: Damage-associated molecular patterns
IL: Interleukin
IRI: Ischemia-reperfusion injury
MI: Myocardial infarction
PCI: Percutaneous coronary intervention
ROS: Reactive oxygen species
TNF-α: Tumor necrosis factor-alpha
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How to Cite This Article
Yasemin Hacanlı. Mechanism of cardiac damage: ischemia-reperfusion injury. Eu Clin Anal Med 2025;13(2):53. doi:10.4328/ECAM.10108
- Received:
- 04.01.2025
- Accepted:
- 14.01.2025
- Published Online:
- 18.01.2025
- Printed:
- 01.05.2025
![Figure 1. Mechanisms of myocardial damage in cardiac surgery and factors that increase this damage [12]](https://eurasianmedicine.com/archive/vol13/issue2/10.4328-ECAM.10108/figure-1.png)