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Mitochondrial Transplantation for Cardioprotection and Induction of Angiogenesis in Ischemic Heart Disease Publisher Pubmed



Hassanpour P1, 2 ; Sadeghsoltani F1 ; Saghebasl S1 ; Boroumand S3 ; Khanicheragh P4 ; Tafti SHA3 ; Rahbarghazi R1, 5 ; Rahmati M1, 2
Authors
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Authors Affiliations
  1. 1. Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
  2. 2. Department of Clinical Biochemistry and Laboratory Medicine, Tabriz University of Medical Sciences, Tabriz, 5166614766, Iran
  3. 3. Research Center for Advanced Technologies In Cardiovascular Medicine, Cardiovascular Diseases Research Institute, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Student Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
  5. 5. Department of Applied Cell Sciences, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, 5166653431, Iran

Source: Stem Cell Research and Therapy Published:2025


Abstract

To date, the regenerative potential of mitochondrial transplantation (MT) has been extensively investigated under several pathologies. Among various cardiovascular diseases, ischemic heart disease (IHD), the most prevalent pathological condition in human medicine, is induced by coronary artery narrowing, or occlusion, leading to bulk necrotic changes and fibrosis within the myocardium. Data associated with the pro-angiogenic activity of mitochondria have not been completely elucidated in terms of cardiac tissue regeneration. Here, we aimed to highlight the recent studies and advantages related to the application of mitochondrial mass in the ischemic myocardium. How and by which mechanisms, mitochondria can reduce aberrant myocardial tissue remodeling via different pathways such as angiogenesis and de novo blood formation was discussed in detail. We hope that data from the current review article help us understand the molecular and cellular mechanisms by which transplanted mitochondria exert their regenerative properties in the ischemic myocardium. © The Author(s) 2025.
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