Table 2: PPAR mouse animal models.

TargetModelCardiac metabolismCardiac functionReference

PPARαPPARα−/−Defective lipid and glucose homeostasis[116]
Defective lipid homeostatic response to fasting [106]
Decreased FAO, abnormal mitochondriaFibrosis, progressed during aging[117]
Decreased FAO, increased glucose oxidation and glycolysisNormal cardiac function[118]
Substrate switch from fatty acid to glucose, inefficient ATP generationNormal cardiac function[120]
Systolic ventricular dysfunction, fibrosis[121]
Increased oxidative stress, LV dysfunction[122, 123]
Decreased FAO, increased glucose oxidationNormal cardiac function[119]
αMHC-PPARαIncreased FAO, decreased glucose oxidation and uptakeVentricular hypertrophy, systolic ventricular dysfunction[107]

PPARδPPARδ−/−Impaired development [134]
Embryonic lethality [133]
αMHC-PPARδ−/−Decreased FAO and increased glucose oxidation, lipid accumulationCardiac dysfunction, hypertrophy, and reduced survival[115]
Decreased FAO and normal glucose oxidationHypertrophy, mitochondrial abnormalities, and cardiac dysfunction[137]
Inducible αMHC-PPARδ−/−Decreased FAO and glucose oxidation, mitochondrial abnormalitiesCardiac dysfunction, oxidative damage, and hypertrophy [135]
αMHC-PPARδNormal FAO, increased glucose oxidation Normal cardiac function[136]
Inducible αMHC-PPARδIncreased FAO and glucose oxidation, increased mtDNAEnhanced cardiac contractility[137]

PPARγPPARγ−/−Embryonic lethality [126]
αMHC-PPARγ−/−Hypertrophy, preserved systolic function[127]
Hypertrophy, mitochondrial oxidative damage, and dilated cardiomyopathy[131]
No changes in cardiac metabolism at baseline[129]
Inducible αMHC-PPARγ−/−Decreased FAO, normal glucose oxidationDecreased cardiac contractility, modest hypertrophy[132]
MLC2v-PPARγ−/−Hypertrophy, macrophage infiltration[128]
αMHC-PPARγ1Increased TG uptake, increased lipid and glycogen stores, and abnormal mitochondriaDilated cardiomyopathy[113]
MLC2v-PPARγIncreased cardiomyocyte length[130]