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. Author manuscript; available in PMC: 2020 Oct 1.
Published in final edited form as: J Neurovirol. 2019 Jan 22;25(5):722–733. doi: 10.1007/s13365-019-00721-6

Figure 1. Schematic representation of the proposed metabolic switch in astrocytic metabolism during treatment with recombinant HIV-1 Tat protein.

Figure 1.

Left panel: Under neurotrophic conditions, astrocytes primarily utilize anaerobic glycolysis resulting in the conversion on pyruvate to lactate by lactate dehydrogenase (LDH) which then is released from the cell via monocarboxylate transporter 4 (MCT4) into the extracellular compartment. Right panel: Under conditions of cell stress such as HIV-1 Tat insult, astrocytes take on a neurotoxic phenotype in which pyruvate is no longer converted to lactate. Instead, pyruvate is converted into acetyl CoA. Additionally, there is an increase in intracellular calcium into the mitochondria via the mitochondrial calcium uniporter (MCU) and an upregulation of fatty acid oxidation (FAO), providing an additional source of acetyl CoA, which fuels the TCA cycle and drives mitochondrial metabolism within astrocytes. Overall this results in increased production of mitochondrial ROS (mROS) and reduced supply of lactate.