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It is well documented that PPAR  α   and PPAR  β  /  δ   share overlapping functions in regulating myocardial lipid metabolism. However, previous studies demonstrated that cardiomyocyte-restricted PPAR  β  /  δ   deficiency in mice leads to severe cardiac pathological development, whereas global PPAR  α   knockout shows a benign cardiac phenotype. It is unknown whether a PPAR  α  -null background would alter the pathological development in mice with cardiomyocyte-restricted PPAR  β  /  δ   deficiency. In the present study, a mouse model with long-term PPAR  β  /  δ   deficiency in PPAR  α  -null background showed a comparably reduced cardiac expression of lipid metabolism to those of single PPAR-deficient mouse models. The PPAR  α  -null background did not rescue or aggravate the cardiac pathological development linked to cardiomyocyte-restricted PPAR  β  /  δ   deficiency. Moreover, PPAR  α  -null did not alter the phenotypic development in adult mice with the short-term deletion of PPAR  β  /  δ   in their hearts, which showed mitochondrial abnormalities, depressed cardiac performance, and cardiac hypertrophy with attenuated expression of key factors in mitochondrial biogenesis and defense. The present study demonstrates that cardiomyocyte-restricted deletion of PPAR  β  /  δ   in PPAR  α  -null mice causes impaired mitochondrial biogenesis and defense, but no further depression of fatty acid oxidation. Therefore, PPAR  β  /  δ   is essential for maintaining mitochondrial biogenesis and defense in cardiomyocytes independent of PPAR  α  .

ppar research

Cardiomyocyte-Restricted Deletion of PPARβ/δin PPARα-Null Mice Causes Impaired Mitochondrial Biogenesis and Defense, but No Further Depression of Myocardial Fatty Acid Oxidation