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. 2022 Dec 5;18:100512. doi: 10.1016/j.mtbio.2022.100512

Fig. 15.

Fig. 15

The schematic of PEVs regulating mitochondrial function to promote the repair of impaired mitochondria. Glycolysis, oxidative phosphorylation, and the AMPK–SIRT1–PGC1α–TFAM pathway helps to maintain an optimal level of mitochondrial function and intracellular homeostasis in healthy NP cells. In degenerated NP cells, oxidative distress damage and reactive oxygen species (ROS) accumulate, causing damage to the mitochondria, thereby inhibiting AMPK signaling and activity, downregulating SIRT1, decreasing levels of PGC1α and TFAM, and further impairing the mitochondrial function in NP cells. GLUT1, glucose transporter type 1; TCA, tricarboxylic acid; ETC, electron transport chain; ROS, reactive oxygen species; ATP, adenosine-5′-triphosphate; AMPK, AMP-activated protein kinase; SIRT1, NAD-dependent protein deacetylase sirtuin-1; PGC1α, peroxisome proliferator-activated receptor γ co-activator 1α; TFAM, Mt transcription factor A; Nrf1, nuclear respiratory factor 1; Nrf2, nuclear respiratory factor 2; PEVs, platelet-derived extracellular vesicles; SRT-1720, the selective SIRT1 activator; EX-527, the selective SIRT1 inhibitor.