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. Author manuscript; available in PMC: 2022 Mar 28.
Published in final edited form as: Nat Rev Nephrol. 2020 Nov 24;17(5):299–318. doi: 10.1038/s41581-020-00369-0

Fig. 6 |. Targeting mitochondrial quality control mechanisms to protect against kidney injury and accelerate kidney repair in AKI and CKD.

Fig. 6 |

Potential kidney-protective strategies include inhibition of mitochondrial fragmentation using mdivi-1, augmentation of mitochondrial antioxidant capacity using mitochondrial-target antioxidants (for example, SS-31, mitoQ and SkQR1), enhancement of mitophagy using urolithin A or TAT-beclin 1 peptide, enhancement of mitochondrial biogenesis using AMP-activated protein kinase (AMPK) activators (5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) or metformin), sirtuin 1 (SIRT1) activators (SRT1720, resveratrol and quercetin), a 5-hydroxytryptamine receptor 1F (5-HT1F) agonist (LY344864), a β2 adrenergic receptor agonist (formoterol) or thiazolidinediones (rosiglitazone and pioglitazone), and augmentation of mitochondrial oxidative metabolism using mitochonic acid 5, SS-31 or niacinamide. AKI, acute kidney injury; CKD, chronic kidney disease; ROS, reactive oxygen species.