Cardioprotection via mitochondrial transplantation supports fatty acid metabolism in ischemia-reperfusion injured rat heartopen access
- Authors
- 장지희; 강기운; 김영원; 정서현; 박재윤; 박지훈; 문지성; 장정현; 김서현; 김성훈; 조성주; 이유림; 김형규; 한진; 고은아; 정성철; 김정하; 고재홍
- Issue Date
- May-2024
- Publisher
- 대한약리학회
- Keywords
- Autografts; Mitochondria; Myocardial ischemia; Myocardial reperfusion; Oxygen consumption; Transplantation
- Citation
- The Korean Journal of Physiology & Pharmacology, v.28, no.3, pp 209 - 217
- Pages
- 9
- Journal Title
- The Korean Journal of Physiology & Pharmacology
- Volume
- 28
- Number
- 3
- Start Page
- 209
- End Page
- 217
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/73834
- DOI
- 10.4196/kjpp.2024.28.3.209
- ISSN
- 1226-4512
2093-3827
- Abstract
- In addition to cellular damage, ischemia-reperfusion (IR) injury induces substantial damage to the mitochondria and endoplasmic reticulum. In this study, we sought to determine whether impaired mitochondrial function owing to IR could be restored by transplanting mitochondria into the heart under ex vivo IR states. Additionally, we aimed to provide preliminary results to inform therapeutic options for ischemic heart disease (IHD). Healthy mitochondria isolated from autologous gluteus maximus muscle were transplanted into the hearts of Sprague–Dawley rats damaged by IR using the Langendorff system, and the heart rate and oxygen consumption capacity of the mitochondria were measured to confirm whether heart function was restored. In addition, relative expression levels were measured to identify the genes related to IR injury. Mitochondrial oxygen consumption capacity was found to be lower in the IR group than in the group that underwent mitochondrial transplantation after IR injury (p < 0.05), and the control group showed a tendency toward increased oxygen consumption capacity compared with the IR group. Among the genes related to fatty acid metabolism, Cpt1b (p < 0.05) and Fads1 (p < 0.01) showed significant expression in the following order: IR group, IR + transplantation group, and control group. These results suggest that mitochondrial transplantation protects the heart from IR damage and may be feasible as a therapeutic option for IHD.
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