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Several evidences have demonstrated the contribution of these alterations to pathophysiological states related to mitochondrial dysfunction, such as: (1) the inhibition of CI in human cells causes an upregulation of the mRNA levels of CBS and CSE , together with the upregulation of PSAT1 , SHMT2 and PHGDH , which are involved in serine/glycine biosynthesis and folate cycle [71], (2) the levels of the MTHF2 protein, involved in the folate cycle, are increased in the Deletor mouse model, a mouse model with accumulation of mtDNA deletions, resulting in modifications in one-carbon metabolism [72], (3) the levels of MTHF2 and SHTM2 proteins are increased in other mouse models of mitochondrial diseases caused by defects in mtDNA [7], (4) CBS , CSE , PHGDGH , PSPH and PSAT1 mRNAs are upregulated in other human cell models of pharmacologically induced mtDNA depletion [73] and (5) MTHFD1 L, MTHFD2 , PSAT1 and PHGDH are upregulated in patients with mitochondrial myopathy caused by mtDNA deletion [70]

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Neurosci Lett 10(12):171174 Sonnewald U, Westergaard N, Schousboe A, Svendsen JS, Unsgard G, Petersen SB (1993) Direct demonstration by [13C]NMR spectroscopy that glutamine from astrocytes is a precursor for GABA synthesis in neurons

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