Key result
In a mouse model of repetitive ischemia/reperfusion, downregulation of PPARalpha was mediated by reactive oxygen species and served as an adaptive mechanism to prevent cardiac lipotoxicity.
Why the study?
Does downregulation of PPARalpha prevent lipotoxicity and maintain contractile function in a mouse model of repetitive ischemia/reperfusion?
Population
C57/BL6 mice, mice overexpressing extracellular superoxide dismutase, and mice treated with the PPARalpha…
Comparison
Repetitive closed-chest I/R, overexpression of… vs Wild-type mice or mice not exposed to EC-SOD…
Design
Preclinical
Follow-up
Up to 28 days of repetitive I/R and 30 days after…
Authors
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ROS-mediated PPARalpha downregulation may prevent lipotoxicity in repetitive I/R; hypothesis-generating in mice, no clinical implications yet.
Does downregulation of PPARalpha prevent lipotoxicity and maintain contractile function in a mouse model of repetitive ischemia/reperfusion?
Downregulation of PPARalpha during repetitive ischemia/reperfusion is a reactive oxygen species-dependent adaptive mechanism that prevents cardiac lipotoxicity.
Dewald et al. (2005) studied Ischemic cardiomyopathy. Repetitive ischemia/reperfusion (I/R) vs. Discontinuation of I/R, overexpression of EC-SOD, or PPARalpha agonist WY-14,643 was evaluated on Echocardiography, histology, and candidate gene expression. In a mouse model of repetitive ischemia/reperfusion, downregulation of PPARalpha was mediated by reactive oxygen species and served as an adaptive mechanism to prevent cardiac lipotoxicity.
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