Mesenchymal stem cell therapy targeting mitochondrial dysfunction in acute kidney injury

Table 1 Associated articles demonstrating the mechanisms by which MSC therapy target mitochondrial dysfunction in AKI

Year	Animal	AKI model	MSCs source	Outcomes	References
2017	Mice	Glycerol	Bone marrow	↑ATP, ↑Activation of PI3K/Akt pathway; ↓ROS, ↓Mitochondrial-apoptosis related proteins, ↓Cell apoptosis	Geng et al. [64]
2013	Rats	Cisplatin	Umbilical cord	↓Activation of mitochondrial apoptosis signaling, ↓MDA	Peng et al. [65]
2017	Rats	Cisplatin	Bone marrow	↑PGC-1α, ↑Activation of wnt/β-catenin pathway; ↓ROS	Jiao et al. [66]
2016	Rats	I/R	Wharton Jelly	↑miR-30; ↓Mitochondrial fssion, ↓Cell apoptosis	Gu et al. [68]
2017	Mice	Cisplatin	Umbilical cord	↑ATP, ↑PGC-1α, ↑NAD+, ↑SIRT3; ↑Mitochondrial exchange ↓ROS; Normalized mitochondrial shape, density and mass	Perico et al. [70]

MSCs mesenchymal stem cells, AKI acute kidney injury, I/R ischemia/reperfusion, ATP adenosine triphosphate, ROS reactive oxygen species, MDA malondialdehyde, PGC-1α peroxisome proliferator-activated receptor-γ coactivator-1α, SIRT3 sirtuin 3

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