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The citric acid cycle, also known as the Krebs cycle or tricarboxylic acid (TCA) cycle, is a central metabolic pathway occurring in the mitochondrial matrix of eukaryotic cells (and cytosol of prokaryotes), in which acetyl-CoA derived from carbohydrates, fats, and proteins is oxidized to carbon dioxide, generating reducing equivalents (NADH, FADH₂) for ATP production via oxidative phosphorylation. The cycle also provides intermediates for amino acid synthesis, heme synthesis, and other biosynthetic processes, reflecting its role as an amphibolic (both anabolic and catabolic) pathway. While not a specific molecular target, defects in individual cycle enzymes are implicated in several diseases, and some drugs or therapeutic strategies attempt to target specific enzymes or metabolic nodes within or feeding into the citric acid cycle.
Inhibition of glutaminolysis, Inhibition or correction of cycle enzyme mutations, Modulation of substrate availability (e.g., α-ketoglutarate supplementation), Correction of metabolic defects in enzyme deficiencies
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