ArticlebioRxiv : the preprint server for biology2026
Loss of TAFAZZIN leads to perturbation of amino acid metabolism and reduction of collagen synthesis.
Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Barth syndrome is a life-threatening genetic disorder caused by mutations in the TAFAZZIN (TAZ) gene, which disrupt remodeling of cardiolipin in mitochondria. The disease is associated with cardiac and skeletal myopathy, neutropenia, fatigue, and metabolic dysfunction. Previous studies showed that loss of TAZ decreases pyruvate dehydrogenase activity, reduces glucose flux into the TCA cycle, and impairs fatty acid metabolism. To test the hypothesis that amino acid (AA) metabolism may be altered to compensate for these deficiencies, we characterized AA metabolism in TAZ-deficient mouse myoblasts (TAZ-KO). Levels of branched-chain amino acids (BCAAs) were reduced, while proline levels were increased in TAZ-KO cells. Levels of proline dehydrogenase and glutamate dehydrogenase, which convert proline to TCA cycle intermediates, were increased.
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