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Mitochondrial Transplantation Ameliorates Ischemia/Reperfusion-Induced Kidney Injury in Rat Publisher Pubmed



Jabbari H1 ; Roushandeh AM1, 2 ; Rostami MK1 ; Razavitoosi MT1 ; Shokrgozar MA3 ; Jahaniannajafabadi A4, 5 ; Kuwahara Y6 ; Roudkenar MH7
Authors
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Authors Affiliations
  1. 1. Medical Biotechnology Department, Paramedicine faculty, Guilan University of Medical Sciences, Rasht, Iran
  2. 2. Anatomical Sciences Department, Medicine Faculty, Guilan University of Medical Sciences, Rasht, Iran
  3. 3. National Cell Bank of Iran, Pasteur Institute of Iran, Tehran, Iran
  4. 4. Department of Pharmaceutical Biotechnology, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran
  5. 5. Department of Applied Pharmacology, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima, 890-8544, Japan
  6. 6. Division of Radiation Biology and Medicine, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Sendai, Japan
  7. 7. Cardiovascular Diseases Research Center, Department of Cardiology, Heshmat Hospital, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran

Source: Biochimica et Biophysica Acta - Molecular Basis of Disease Published:2020


Abstract

No real therapeutic modality is currently available for Acute kidney injury (AKI) and if any, they are mainly supportive in nature. Therefore, developing a new therapeutic strategy is crucial. Mitochondrial dysfunction proved to be a key contributor to renal tubular cell death during AKI. Thus, replacement or augmentation of damaged mitochondria could be a proper target in AKI treatment. Here, in an animal model of AKI, we auto-transplanted normal mitochondria isolated from healthy muscle cells to injured kidney cells through injection to renal artery. The mitochondria transplantation prevented renal tubular cell death, restored renal function, ameliorated kidney damage, improved regenerative potential of renal tubules, and decreased ischemia/reperfusion-induced apoptosis. Although further studies including clinical trials are required in this regard, our findings suggest a novel therapeutic strategy for treatment of AKI. Improved quality of life of patients suffering from renal failure and decreased morbidity and mortality rates would be the potential advantages of this therapeutic strategy. © 2020 Elsevier B.V.
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