The normal functioning of human body requires a steady flow of energy. This energy in the form of adenosine triphosphate (ATP) is produced by breaking down carbon sources like glucose, lipids, or amino acids. The tricarboxylic acid (TCA) cycle, one of the most important ATP-producing processes in the mitochondria, is a major hub of metabolites and is known for ensuring a fine balance between its cyclic intermediates, referred to as the ‘metabolic flux.’ There is a general consensus that this metabolic flux is impaired in heart-related disorders. A common example is myocardial ischemia (MI), a condition in which blood flow to the heart is reduced, preventing the heart muscles, or cardiomyocytes, from receiving enough oxygen. While it is well understood that MI is marked by decreased ATP synthesis and increased glucose breakdown, or “glycolysis,” manipulating the complex TCA cycle to develop treatment options is extremely difficult.