Mitochondrial apoptosis in response to cardiac ischemia-reperfusion injury
Abstract In patients with acute myocardial infarction (AMI), thrombolytic therapy and revascularization strategies allow complete recanalization of occluded epicardial coronary arteries. However, approximately 35% of patients still experience myocardial ischemia/reperfusion (I/R) injury, which contr...
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| Format: | Article |
| Language: | English |
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BMC
2025-01-01
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| Series: | Journal of Translational Medicine |
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| Online Access: | https://doi.org/10.1186/s12967-025-06136-8 |
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| author | Kaixin Wang Qing Zhu Wen Liu Linyuan Wang Xinxin Li Cuiting Zhao Nan Wu Chunyan Ma |
| author_facet | Kaixin Wang Qing Zhu Wen Liu Linyuan Wang Xinxin Li Cuiting Zhao Nan Wu Chunyan Ma |
| author_sort | Kaixin Wang |
| collection | DOAJ |
| description | Abstract In patients with acute myocardial infarction (AMI), thrombolytic therapy and revascularization strategies allow complete recanalization of occluded epicardial coronary arteries. However, approximately 35% of patients still experience myocardial ischemia/reperfusion (I/R) injury, which contributing to increased AMI mortality. Therefore, an accurate understanding of myocardial I/R injury is important for preventing and treating AMI. The death of each cell (cardiomyocytes, endothelial cells, vascular smooth muscle cells, cardiac fibroblasts, and mesenchymal stem cells) after myocardial ischemia/reperfusion is associated with apoptosis due to mitochondrial dysfunction. Abnormal opening of the mitochondrial permeability transition pore, aberrant mitochondrial membrane potential, Ca2+ overload, mitochondrial fission, and mitophagy can lead to mitochondrial dysfunction, thereby inducing mitochondrial apoptosis. The manifestation of mitochondrial apoptosis varies according to cell type. Here, we reviewed the characteristics of mitochondrial apoptosis in cardiomyocytes, endothelial cells, vascular smooth muscle cells, cardiac fibroblasts, and mesenchymal stem cells following myocardial ischemia/reperfusion. |
| format | Article |
| id | doaj-art-ae05d114671646dfb6e97533f6dee66e |
| institution | Kabale University |
| issn | 1479-5876 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | BMC |
| record_format | Article |
| series | Journal of Translational Medicine |
| spelling | doaj-art-ae05d114671646dfb6e97533f6dee66e2025-02-02T12:40:26ZengBMCJournal of Translational Medicine1479-58762025-01-0123111210.1186/s12967-025-06136-8Mitochondrial apoptosis in response to cardiac ischemia-reperfusion injuryKaixin Wang0Qing Zhu1Wen Liu2Linyuan Wang3Xinxin Li4Cuiting Zhao5Nan Wu6Chunyan Ma7Department of Cardiovascular Ultrasound, The First Hospital of China Medical UniversityDepartment of Cardiovascular Ultrasound, The First Hospital of China Medical UniversityDepartment of Cardiovascular Ultrasound, The First Hospital of China Medical UniversityDepartment of Cardiovascular Ultrasound, The First Hospital of China Medical UniversityDepartment of Cardiovascular Ultrasound, The First Hospital of China Medical UniversityDepartment of Cardiovascular Ultrasound, The First Hospital of China Medical UniversityThe Central Laboratory of The First Affiliated Hospital of China Medical UniversityDepartment of Cardiovascular Ultrasound, The First Hospital of China Medical UniversityAbstract In patients with acute myocardial infarction (AMI), thrombolytic therapy and revascularization strategies allow complete recanalization of occluded epicardial coronary arteries. However, approximately 35% of patients still experience myocardial ischemia/reperfusion (I/R) injury, which contributing to increased AMI mortality. Therefore, an accurate understanding of myocardial I/R injury is important for preventing and treating AMI. The death of each cell (cardiomyocytes, endothelial cells, vascular smooth muscle cells, cardiac fibroblasts, and mesenchymal stem cells) after myocardial ischemia/reperfusion is associated with apoptosis due to mitochondrial dysfunction. Abnormal opening of the mitochondrial permeability transition pore, aberrant mitochondrial membrane potential, Ca2+ overload, mitochondrial fission, and mitophagy can lead to mitochondrial dysfunction, thereby inducing mitochondrial apoptosis. The manifestation of mitochondrial apoptosis varies according to cell type. Here, we reviewed the characteristics of mitochondrial apoptosis in cardiomyocytes, endothelial cells, vascular smooth muscle cells, cardiac fibroblasts, and mesenchymal stem cells following myocardial ischemia/reperfusion.https://doi.org/10.1186/s12967-025-06136-8Ischemia/reperfusion injuryMitochondrial apoptosisCardiomyocyteEndothelial cell |
| spellingShingle | Kaixin Wang Qing Zhu Wen Liu Linyuan Wang Xinxin Li Cuiting Zhao Nan Wu Chunyan Ma Mitochondrial apoptosis in response to cardiac ischemia-reperfusion injury Journal of Translational Medicine Ischemia/reperfusion injury Mitochondrial apoptosis Cardiomyocyte Endothelial cell |
| title | Mitochondrial apoptosis in response to cardiac ischemia-reperfusion injury |
| title_full | Mitochondrial apoptosis in response to cardiac ischemia-reperfusion injury |
| title_fullStr | Mitochondrial apoptosis in response to cardiac ischemia-reperfusion injury |
| title_full_unstemmed | Mitochondrial apoptosis in response to cardiac ischemia-reperfusion injury |
| title_short | Mitochondrial apoptosis in response to cardiac ischemia-reperfusion injury |
| title_sort | mitochondrial apoptosis in response to cardiac ischemia reperfusion injury |
| topic | Ischemia/reperfusion injury Mitochondrial apoptosis Cardiomyocyte Endothelial cell |
| url | https://doi.org/10.1186/s12967-025-06136-8 |
| work_keys_str_mv | AT kaixinwang mitochondrialapoptosisinresponsetocardiacischemiareperfusioninjury AT qingzhu mitochondrialapoptosisinresponsetocardiacischemiareperfusioninjury AT wenliu mitochondrialapoptosisinresponsetocardiacischemiareperfusioninjury AT linyuanwang mitochondrialapoptosisinresponsetocardiacischemiareperfusioninjury AT xinxinli mitochondrialapoptosisinresponsetocardiacischemiareperfusioninjury AT cuitingzhao mitochondrialapoptosisinresponsetocardiacischemiareperfusioninjury AT nanwu mitochondrialapoptosisinresponsetocardiacischemiareperfusioninjury AT chunyanma mitochondrialapoptosisinresponsetocardiacischemiareperfusioninjury |