Korean J Physiol Pharmacol 2024; 28(3): 209-217
Published online May 1, 2024 https://doi.org/10.4196/kjpp.2024.28.3.209
Copyright © Korean J Physiol Pharmacol.
Jehee Jang1,#, Ki-Woon Kang2,#, Young-Won Kim1, Seohyun Jeong1, Jaeyoon Park3, Jihoon Park3, Jisung Moon3, Junghyun Jang3, Seohyeon Kim3, Sunghun Kim3, Sungjoo Cho3, Yurim Lee3, Hyoung Kyu Kim4, Jin Han4, Eun-A Ko5, Sung-Cherl Jung5, Jung-Ha Kim6,*, and Jae-Hong Ko1,*
1Department of Physiology, College of Medicine, Chung-Ang University, Seoul 06974, 2Divsion of Cardiology, Department of Internal Medicine, College of Medicine, Chung-Ang University Hospital, Seoul 06973, 3Department of Medicine, College of Medicine, Chung-Ang University, Seoul 06974, 4Cardiovascular and Metabolic Disease Center, SMART Marine Therapeutics Center, Inje University, Busan 47392, 5Department of Physiology, School of Medicine, Jeju National University, Jeju 63243, 6Department of Family Medicine, College of Medicine, Chung-Ang University Hospital, Seoul 06973, Korea
Correspondence to:Jung-Ha Kim
E-mail: girlpower219@cau.ac.kr
Jae-Hong Ko
E-mail: akdongyi01@cau.ac.kr
#These authors contributed equally to this work.
Author contributions: All authors read and approved the final manuscript. J.J., K.W.K., and Y.W.K.: Conceptualization, Data curation, Formal analysis, Writing – original draft, Writing – review & editing. J.J. and K.W.K.: Visualization. J.J., S.J., J.Y.P., J.H.P., J.M., J.J.3, S.Hy.K., S.Hu.K., S.J.C., and Y.L.: Investigation, Writing – review & editing. K.W.K. and Y.W.K.: Resources, Project administration. H.K.K., J.H., E.A.K., and S.C.J.: Project administration, Formal analysis, Writing – review & editing. J.H.K.6 and J.H.K.: Conceptualization, Funding acquisition, Supervision, Writing – original draft, Writing – review & editing.
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.
Keywords: Autografts, Mitochondria, Myocardial ischemia, Myocardial reperfusion, Oxygen consumption, Transplantation
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