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. 2022 Sep 23;9:1017650. doi: 10.3389/fmed.2022.1017650

Figure 2.

Figure 2

Mitochondrial homeostasis and T-cell energy metabolism. Both glycolysis and FAO mediate T-cell energy metabolism. Deficiency of MRE11A and NMT1 and oxidative phosphorylation during glycolysis metabolism in RA synoviocytes promote the leakage of mtDNA from mitochondria, leading to the secretion of inflammatory substances. During FAO in RA synoviocytes, abnormal activation of AMPK phosphorylation of ACC leads to mitochondrial citric acid transport to the cytoplasm, mediating the secretion of inflammatory substances. Additionally, it activates mTOR, which inhibits mitochondrial autophagy.