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MOTS-C has been investigated for its interaction with mitochondrial signaling networks and cellular metabolic communication mechanisms

These effects were dose-dependent and particularly pronounced at higher doses

-Aminobutyric acid-A (GABA-A), amyloid beta (A), peroxisome proliferator-activated, receptor-gamma coactivator-1 (PGC-1), PTEN-induced putative kinase 1 (PINK1), reactive oxygen species (ROS), sirtuin 1 (SIRT1), nuclear factor kappa-light-chain-enhancer of activated cells (NF-kB), forkhead box O (FOXO), diabetic autonomic neuropathy, tumor necrosis factor (TNF), interleukin-1 (IL-1), interleukin-6 (IL-6), advanced glycation end products (AGE), protein kinase C (PKC), N-methyl-D-aspartate (NMDA), bloodbrain barrier (BBB), insulin receptor (IR), phosphorylated Tau, acetylcholinesterase (AChE), superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), malonaldehyde (MDA), low-density lipoproteins-cholesterol (LDL-C), hemoglobin A1c (HbAlc), and glycogen synthase kinase-3 beta (GSK3B)