Key result
Overexpression of ACOT1 in diabetic mice significantly attenuated cardiac dysfunction and reduced oxidative stress via repression of the PPARα/PGC1α signaling pathway.
Why the study?
Does ACOT1 overexpression improve cardiac function and reduce oxidative stress in diabetic mouse models?
Does ACOT1 overexpression improve cardiac function and reduce oxidative stress in diabetic mouse models?
Absolute Event Rate: 85.5% vs 78.1%
p-value: p=<0.01
ACOT1 overexpression protects against diabetic cardiomyopathy by reducing oxidative stress and reversing altered myocardial energy substrate use via the PPARα/PGC1α signaling pathway.
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ACOT1 overexpression may protect against diabetic cardiomyopathy in mice; hypothesis-generating and leaves open human translation.
Yang et al. (2012) studied Diabetic cardiomyopathy (n=63). ACOT1 overexpression (pcDNA3.1-Acot1) vs. Empty vector (pcDNA3.1) or untreated control was evaluated on Left ventricular ejection fraction (LVEF) (p=<0.01). Overexpression of ACOT1 in diabetic mice significantly attenuated cardiac dysfunction and reduced oxidative stress via repression of the PPARα/PGC1α signaling pathway.
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