Skip to main content
. 2024 Aug 13;7:180. doi: 10.1038/s42004-024-01256-6

Fig. 1. Influence of mitochondrial respiration on the carcinogenesis.

Fig. 1

Increased activity of STAT3 and NF-kB signaling can enhance mitochondrial respiration and oxidative phosphorylation, leading to increased ATP production. Elevated ATP levels support cell migration and the activity of P-gp and HSPs, which can reduce the effectiveness of chemotherapy and PTT, respectively. Higher ΔΨm can promote the production of reactive oxygen species (ROS), contributing to tumor development, metastatic activity, and immunosuppression. Heightened mitochondrial activity may also lead to decreased oxygen levels, initiating hypoxia. HIF-1α (activated by hypoxia), which in turn induces the expression of numerous tumorigenic factors such as VEGF (a stimulator of angiogenesis) and PD-L1 (protection against immune cells). The figure was partly generated using Servier Medical Art, provided by Servier, licensed under a Creative Commons Attribution 3.0 unported license. ΔΨm, mitochondrial membrane potential; HIF-1α, hypoxia inducible factor 1 subunit alpha; HSP, heat shock protein; NF-kB; Nuclear factor NF kappa B; PD-L1, programmed death-ligand 1; PDT, photodynamic therapy; P-gp, P-glycoprotein; PTT, photothermal therapy; ROS, reactive oxygen species; STAT3, signal transducer and activator of transcription 3; VEGF, vascular endothelial growth factor.