Key result
Grx2 deficiency in male mice decreased mitochondrial ATP production by complex I-linked substrates to half that of wild type mitochondria, leading to left ventricular hypertrophy and fibrosis.
Why the study?
Does Grx2 deficiency alter mitochondrial oxidative phosphorylation and induce cardiac pathology in mice?
Population
Male C57BL/6 wild type (WT) and Grx2 whole body knock-out (Grx2-/-) mice aged 9-12 weeks
Comparison
Grx2 deletion (Grx2-/-) vs Wild type (WT) mice
Design
Preclinical
Follow-up
Evaluated at 6, 9-12, and 16 weeks of age
Authors
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Grx2 may modulate cardiac mitochondrial function in mice; hypothesis-generating and leaves open human relevance.
Does Grx2 deficiency alter mitochondrial oxidative phosphorylation and induce cardiac pathology in mice?
Grx2 plays a vital role in modulating mitochondrial metabolism in cardiac muscle, and its deficiency leads to left ventricular hypertrophy and fibrosis due to deregulated glutathionylation.
Mailloux et al. (2014) studied Cardiac hypertrophy and mitochondrial dysfunction. Grx2 deficiency (Grx2-/-) vs. Wild type (WT) mice was evaluated on Mitochondrial ATP production by complex I-linked substrates. Grx2 deficiency in male mice decreased mitochondrial ATP production by complex I-linked substrates to half that of wild type mitochondria, leading to left ventricular hypertrophy and fibrosis.
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