Cardiomyocyte-Restricted Deletion of PPARβδ in PPARα-Null Mice Causes Impaired Mitochondrial Biogenesis and Defense, but No Further Depression of Myocardial Fatty Acid Oxidation
Joint Authors
Brako, Lawrence A.
Qin, Qianhong
Lewis, William
Luo, Jinwen
Li, Yuquan
Cheng, Lihong
He, Lan
Yang, Qinglin
Liu, Jian
Lo, Woo-kuen
Wang, Peiyong
Source
Issue
Vol. 2011, Issue 2011 (31 Dec. 2011), pp.1-13, 13 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2011-09-05
Country of Publication
Egypt
No. of Pages
13
Main Subjects
Natural & Life Sciences (Multidisciplinary)
Biology
Abstract EN
It is well documented that PPARα and PPARβ/δ share overlapping functions in regulating myocardial lipid metabolism.
However, previous studies demonstrated that cardiomyocyte-restricted PPARβ/δ deficiency in mice leads to severe cardiac pathological development, whereas global PPARα knockout shows a benign cardiac phenotype.
It is unknown whether a PPARα-null background would alter the pathological development in mice with cardiomyocyte-restricted PPARβ/δ deficiency.
In the present study, a mouse model with long-term PPARβ/δ deficiency in PPARα-null background showed a comparably reduced cardiac expression of lipid metabolism to those of single PPAR-deficient mouse models.
The PPARα-null background did not rescue or aggravate the cardiac pathological development linked to cardiomyocyte-restricted PPARβ/δ deficiency.
Moreover, PPARα-null did not alter the phenotypic development in adult mice with the short-term deletion of PPARβ/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 PPARβ/δ in PPARα-null mice causes impaired mitochondrial biogenesis and defense, but no further depression of fatty acid oxidation.
Therefore, PPARβ/δ is essential for maintaining mitochondrial biogenesis and defense in cardiomyocytes independent of PPARα.
American Psychological Association (APA)
Liu, Jian& Wang, Peiyong& He, Lan& Li, Yuquan& Luo, Jinwen& Cheng, Lihong…[et al.]. 2011. Cardiomyocyte-Restricted Deletion of PPARβδ in PPARα-Null Mice Causes Impaired Mitochondrial Biogenesis and Defense, but No Further Depression of Myocardial Fatty Acid Oxidation. PPAR Research،Vol. 2011, no. 2011, pp.1-13.
https://search.emarefa.net/detail/BIM-466886
Modern Language Association (MLA)
Liu, Jian…[et al.]. Cardiomyocyte-Restricted Deletion of PPARβδ in PPARα-Null Mice Causes Impaired Mitochondrial Biogenesis and Defense, but No Further Depression of Myocardial Fatty Acid Oxidation. PPAR Research No. 2011 (2011), pp.1-13.
https://search.emarefa.net/detail/BIM-466886
American Medical Association (AMA)
Liu, Jian& Wang, Peiyong& He, Lan& Li, Yuquan& Luo, Jinwen& Cheng, Lihong…[et al.]. Cardiomyocyte-Restricted Deletion of PPARβδ in PPARα-Null Mice Causes Impaired Mitochondrial Biogenesis and Defense, but No Further Depression of Myocardial Fatty Acid Oxidation. PPAR Research. 2011. Vol. 2011, no. 2011, pp.1-13.
https://search.emarefa.net/detail/BIM-466886
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-466886