Key result
Cardiac-restricted overexpression of PPARalpha in mice significantly reduced the recovery of cardiac power after ischemia-reperfusion injury compared to nontransgenic controls (45% vs 71%; P<0.05).
Why the study?
Does chronic activation or deletion of PPARalpha alter cardiac recovery after ischemia-reperfusion injury in isolated mouse hearts?
Population
Isolated working hearts from mice with cardiac-restricted overexpression of PPARalpha or whole body…
Comparison
Cardiac-restricted overexpression of PPARalpha… vs Nontransgenic littermates or wild-type hearts
Design
Preclinical
Authors
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PPARalpha overexpression impairs postischemic recovery in mouse hearts; hypothesis-generating for PPARalpha modulation in clinical ischemia-reperfusion injury.
Does chronic activation or deletion of PPARalpha alter cardiac recovery after ischemia-reperfusion injury in isolated mouse hearts?
Absolute Event Rate: 45% vs 71%
p-value: p=<0.05
Chronic activation of PPARalpha increases fatty acid oxidation and is detrimental to cardiac recovery during reperfusion after ischemia in a mouse model.
Sambandam et al. (2005) studied Myocardial ischemia-reperfusion injury. Cardiac-restricted overexpression of PPARalpha (MHC-PPARalpha) vs. Nontransgenic (NTG) littermates was evaluated on Recovery of cardiac power (% of preischemic levels) (p=<0.05). Cardiac-restricted overexpression of PPARalpha in mice significantly reduced the recovery of cardiac power after ischemia-reperfusion injury compared to nontransgenic controls (45% vs 71%; P<0.05).
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