Deletion of peroxisome proliferator-activated receptor-α induces an alteration of cardiac functions
Key result
Deletion of PPARalpha in mice reduced left ventricular fractional shortening and contractile force, and induced myocardial fibrosis compared to wild-type mice.
Why the study?
Does deletion of PPARalpha alter cardiac functions in mice?
Population
PPARalpha knockout (PPARalpha -/-) mice
Comparison
Deletion of peroxisome proliferator-activated… vs Wild-type (PPARalpha +/+) mice
Design
Preclinical
Authors
Discussion
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Implication
Impaired cardiac function after PPARalpha deletion in mice leaves open its role as a therapeutic target in human heart failure.
Structured PICO
Does deletion of PPARalpha alter cardiac functions in mice?
P
Population
PPARalpha knockout (PPARalpha -/-) mice
I
Intervention
Deletion of peroxisome proliferator-activated receptor-alpha (PPARalpha)
C
Comparator
Wild-type (PPARalpha +/+) mice
O
Outcome
Cardiac functions including hemodynamic parameters, echocardiographic measurements, electrocardiography, ex vivo myocardial function, and histological analysissurrogate
Deletion of PPARalpha in mice leads to impaired cardiac contractile performance and myocardial fibrosis, highlighting its essential role in maintaining normal cardiac function.
Cite This Study
Loichot et al. (2006) studied Cardiac function and myocardial fibrosis. Deletion of peroxisome proliferator-activated receptor-alpha (PPARalpha -/-) vs. Wild-type (PPARalpha +/+) mice was evaluated on Cardiac functions including hemodynamic, echocardiographic, and contractile performance. Deletion of PPARalpha in mice reduced left ventricular fractional shortening and contractile force, and induced myocardial fibrosis compared to wild-type mice.