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Defective vascular smooth muscle cell tafazzin impairs mitochondrial function and promotes atherosclerosis

ABSTRACT: Atherosclerotic lesions show significant mitochondrial dysfunction but the underlying mechanisms and consequences remain unknown. Cardiolipin is a phospholipid found exclusively in the mitochondrial inner membrane, the site of oxidative phosphorylation. Tafazzin is a trans-acylase that acylates immature monolysocardiolipin to mature cardiolipin. Tafazzin mutations can result in Barths Syndrome, which is characterized by dilated cardiomyopathy, skeletal myopathy and impaired growth. However, a role for tafazzin in atherosclerosis development has not been previously identified. Here we show that tafazzin expression is decreased in atherosclerotic lesions and specifically in plaque vascular smooth muscle cells (VSMCs).

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Albert Koulman

PROVIDER: MSV000099336 | MassIVE |

REPOSITORIES: MassIVE

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Defective mitochondrial cardiolipin remodeling dampens HIF-1a expression in hypoxia

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