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Review
. 2019 May 2;17(1):142.
doi: 10.1186/s12967-019-1893-4.

Mesenchymal stem cell therapy targeting mitochondrial dysfunction in acute kidney injury

Lingfei Zhao  1   2   3 , Chenxia Hu  4 , Ping Zhang  1   2   3 , Hua Jiang  1   2   3 , Jianghua Chen  5   6   7
Affiliations
Review

Mesenchymal stem cell therapy targeting mitochondrial dysfunction in acute kidney injury

Lingfei Zhao et al. J Transl Med. .

Abstract

Mitochondria take part in a network of cellular processes that regulate cell homeostasis. Defects in mitochondrial function are key pathophysiological changes during acute kidney injury (AKI). Mesenchymal stem cells (MSCs) have shown promising regenerative effects in experimental AKI models, but the specific mechanism is still unclear. Some studies have demonstrated that MSCs are able to target mitochondrial dysfunction during AKI. In this review, we summarize these articles, providing an integral and updated view of MSC therapy targeting mitochondrial dysfunction during AKI, which is aimed at promoting the therapeutic effect of MSCs in AKI patients.

Keywords: Acute kidney injury; Mesenchymal stem cells; Mitochondrial dysfunction.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Mitochondrial dysfunction during AKI. During AKI, the mitochondria tend towards fission rather than fusion. Together with the suppression of mitophagy, fragmented mitochondria are observed in the cytoplasm. Downregulation of PGC-1α inhibits the biogenesis of mitochondria. Mitochondrial swelling is regarded as a consequence of MPT, which may subsequently release Cyt C and ROS. Dysoxia is also very common, inducing a reduced generation of ATP and cell apoptosis. PGC-1α peroxisome proliferator-activated receptor-γ coactivator-1α, MPT mitochondrial permeability transition, ATP adenosine triphosphate, Cyt C cytochrome C, ROS reactive oxygen species
Fig. 2
Fig. 2
The mechanism by which MSC therapy targets mitochondrial dysfunction in AKI. MSCs are able to accelerate mitochondrial recovery, minimize mitochondrial injury and transfer healthy mitochondria to injured cells. These actions result in decreased levels of MDA, ROS and Cyt C, accompanied by reduced mitochondrial fission and enhanced mitochondrial biogenesis, finally inducing improved mitochondrial function and a reduction in cell apoptosis. MSCs mesenchymal stem cells, PGC-1α peroxisome proliferator-activated receptor-γ coactivator-1α, SIRT3 sirtuin 3, DRP1 dynamin related protein 1, TNTs tunneling nanotubes, MDA malondialdehyde, ROS reactive oxygen species, Cyt C cytochrome C, ATP adenosine triphosphate
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