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. 2021 Jun 29;11(7):961. doi: 10.3390/biom11070961

Figure 4.

Figure 4

Summary of proteomics findings in PBMCs from ME/CFS patients and healthy individuals. We found reduced expression levels of PDPR, which can lead to lower activation of the PDH. In addition, downregulation of VNN1 and PANK2 could indicate lower cellular CoA levels. Thus, a potential decrease in PDH, VNN1, and PANK2 activities could lead to decreased mitochondrial ATP production and increased lactate production from glycolysis. Accordingly, the upregulation of SLC16A3 has been shown in lactate-exporting glycolytic cells. Further, we found downregulation of ATP5F1E and SLC25A24, which can suggest impaired ATP synthesis. The increased levels of LAMTOR1 and LAMTOR5 observed indicate an upregulation of mTORC1, which could be a compensatory mechanism for the lack of ATP in PBMCs from ME/CFS patients.PBMCs: peripheral blood mononuclear cells. ME/CFS: myalgic encephalomyelitis/chronic fatigue syndrome. PDPR: pyruvate dehydrogenase phosphatase regulatory subunit. PDH: pyruvate dehydrogenase complex. VNN1: Pantetheinase, vascular non-inflammatory molecule-1. PANK2: Panthothenate kinase 2. CoA: coenzyme A. ATP: adenosine triphosphate. SLC16A3: monocarboxylate transporter 4. AT5FIE: ATP synthase F1 subunit epsilon. SLC25A24: calcium-binding mitochondrial carrier protein SCaMC-1. mTORC1: Mammalian target of rapamycin complex 1. LAMTOR 1 and 5: ragulator complex protein LAMTOR1/LAMTOR5.