Mitochondrial Dysfunction
17 DNA Methylation Modifications
Alteration in the Mitochondrial Chondrial Phosphoproteome
extracellular secretion of mitochondrial DNA
Found in muscle biopsies for mito
increased utilization of acetyl-CoA-producing amino acids as alternative substrates for fuelling aerobic metabolism via the TCA cycle
lowered mitochondrial chondrial membrane potential, oxygen consumption, and ATP synthetic capacity
reduced levels of ATP or ATP production
Reduced Oxidative Metabolism
level of complex formation between mTOR and one of its known protein partners, raptor, correlated with overall mitochondrial activity
3 DNA and Genetic/Epigenetic Factors
peripheral mononuclear blood cells (PMBC)
+4 White Blood Cells/Leukocytes/Mast Cells/Immune Cells
1a Decreases in Sphingolipid, glycosphingolipid, phospholipid, purine, microbiome aromatic amino acid and branch chain amino acid metabolites, as well as in flavine adenine nucleotide (FAD) and lathosterol
1 Abnormalities in bioenergetic function
3 Alterations in normal energy metabolic processes and abnormalities in cellular bioenergetics
9 of the Cellular Systems, Common Comorbid Diseases (Common) and Uncommon Causal Diseases (Uncommon)
9 Treatment of the Cellular Systems
10 Peptides and Neuropeptides
15 Receptor tyrosine kinase
Abnormalities of AMPK activation and glucose uptake
Antiviral Pathway Deregulation of Chronic Fatigue Syndrome Induces Nitric Oxide Production in Immune Cells That Precludes a Resolution of the Inflammatory Response
Auto-inflammatory state in the hypothalamus
Chronic Infection, Redox State and Mitochondria
Decreased Cellular Oxygen use
Decreased Mitochondrial Membrane Permeability
Directly Inhibit Mitochondrial Respiration by Increasing Mitochondrial Membrane Permeability
DNA damage from Fluoxedine
EphB and Ephrin-B interactions mediate human mesenchymal stem cell suppression of activated T-cells
Eripheral blood mononuclear cells (PBMCs)
From 'Fix Your Fatigue' by Evan Hirsch, MD
From CFS Unravelled by Dan Neuffer
Hypochlorhydria + Dysbiosis + Chronic inflammation = Acquired Mitochondrial Damage
Iintracellular bacterial infection
Impaired Mitochondrial Pyruvate Oxidation, impaired pyruvate catabolism
Impairment in Oxidative Phosphorylation oxidative phosphorylation (OXPHOS)
Implications for Altered Signaling Pathways.
Ion channels located in the membranes of all cells and many cellular organelles
Less efficient and costly processes of frontal cortex
Loss of Transient Receptor Potential Melastatin 3 ion channel function in natural killer cells from Chronic Fatigue Syndrome/Myalgic Encephalomyelitis patients
Neurosteroidogenic Enzymes
oxidative phosphorylation (OXPHOS)
mTOR pathway plays a significant role in determining both resting oxygen consumption and oxidative capacity
Reactive or Dysfunctioning Astrocytes
Resistance to Thyroid Hormone
Sympathetic Nervous System Regulation of Th Cells in Autoimmunity
The AMP-activated protein kinase (AMPK) signaling pathway
Treatment and Mitochondrial support
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Mitochondrial Dysfunction