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. 2021 Oct 19;22(20):11253. doi: 10.3390/ijms222011253

Figure 2.

Figure 2

Schematic illustration of pathophysiological processes of mitochondrial dysfunction, including alterations of mitochondrial structure, dynamics, biogenesis, organelle crosstalk, and oxidative stress, in the AKI, CKD, and AKI to CKD transition. AKI: acute kidney injury; CKD: chronic kidney disease; ATP: adenosine triphosphate; ΔΨm: mitochondrial membrane potential; Mfn1: mitofusin 1; Opa1: optic atrophy 1; Drp1: dynamin related protein 1; mtDNA: mitochondria DNA; AMPK: AMP-activated protein kinase; PGC-1α: PPARgamma-coactivator-1α; Sirt3: sirtuin 3; NRF1: nuclear respiratory factor 1; NRF2: nuclear respiratory factor 2; MRPL12: mitochondrial ribosomal protein L12; cGAS; cyclic guanosine monophosphate–adenosine monophosphate (GMP–AMP) synthase; STING: stimulator of interferon genes; ER: endoplasmic reticulum; UPR: unfolded protein response; PPARα: peroxisome proliferator–activated receptor-α; IRE1: inositol-requiring enzyme 1; PERK: PRKR-like ER kinase; ATF6α activating transcription factor 6α; XPB1: the X-box binding protein 1; eIF2α: eukaryotic initiation factor 2α; ATF4: activating transcription factor 4; ONOO-: peroxynitrite; O2-:superoxide; SOD: superoxide dismutase; GSH: glutathione; ROS: reactive oxygen species.