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| defects of cardiac mitochondria and mitochondrion-associated membranes in taz-deficient mice, and cardiac muscle and skeletal muscle of tafazzin-deficient mice demonstrate ultrastructural defects, including mitochondrial proliferation, myofibrillar disarray, mitophagy  | |
Tafazzin-knockdown in mice markedly impaired oxygen consumption rates during an exercise, without any significant effect on resting metabolic rates |
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Taz deficiency in mouse embryonic fibroblasts (MEFs) also led to impaired oxidative phosphorylation and severe oxidative stress |