From: Mitochondrial transplantation as a novel therapeutic strategy for cardiovascular diseases
Donors | Condition | Recipients | Mechanism | Outcome | References |
---|---|---|---|---|---|
Human endothelial progenitor cells | Ex vivo | Rat cardiomyocytes | TNTs | The formation of intercellular junctions | Koyanagi et al. [46] |
Human MSCs | In vivo | Rat cardiomyocytes | TNTs | Cell-to-cell crosstalk between MSCs and cardiomyocytes in co-culture | Plotnikov et al. [47] |
MSCs | In vitro | Rat cardio-myoblasts | TNTs and cell fusion | Preserved cardio-myoblasts bioenergetics | Cselenyák et al. [48] |
hBM-MSCs | In vitro | Adult mouse cardiomyocytes | Cell fusion | Metabolic reprogramming, transformation to progenitor state | Acquistapace et al. [49] |
hMSCs | In vitro | Human vascular smooth muscle cells | TNTs | increased MSC proliferation | Vallabhaneni et al. [50] |
hBM-MSCs | In vitro | Human umbilical vein endothelial cells | TNTs | Increased mitochondria biogenesis, decreased cell apoptosis, increased proliferation and finally promoted cell survival | Liu et al. [42] |
BM-MSCs and iPSC-MSCs | In vivo | Mouse cardiomyocytes (doxorubicin-induced damage) | TNTs | Increased ATP production and mitochondria biogenesis, increased cell viability and decreased apoptosis | Zhang et al. [51] |
BM-MSCs | In vitro | Rat cardiomyocytes | TNTs | Restored mitochondrial function, decreased cell apoptosis | Han et al. [52] |
hMADSs | In vitro and in vivo | Cardiomyocytes and endothelial cells | TNTs | Increased mitochondrial biogenesis, decreased cell apoptosis | Mahrouf-Yorgov et al. [53] |