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Peroxisome proliferator-activated receptor gamma coactivator-1 promotes cardiac mitochondrial biogenesis.
TLDR
It is found that PGC-1 gene expression is induced in the mouse heart after birth and in response to short-term fasting, conditions known to increase cardiac mitochondrial energy production. Expand
PPAR signaling in the control of cardiac energy metabolism.
TLDR
PPARalpha not only serves a critical role in normal cardiac metabolic homeostasis, but alterations in PPARalpha signaling likely contribute to the pathogenesis of a variety of disease states. Expand
Myocardial recovery and the failing heart: myth, magic, or molecular target?
TLDR
The literature suggests that there are important differences between these 2 phenomena and that myocardial recovery and reverse remodeling are not synonymous, and this review discusses the biology of cardiac remodeling, cardiac reverse remodelling, and myocardIAL recovery with the intent to provide a conceptual framework for understanding myocardials recovery. Expand
Deactivation of peroxisome proliferator-activated receptor-alpha during cardiac hypertrophic growth.
TLDR
Results indicate that during cardiac hypertrophic growth, PPARalpha is deactivated at several levels, leading to diminished capacity for myocardial lipid and energy homeostasis. Expand
p38 Mitogen-activated Protein Kinase Activates Peroxisome Proliferator-activated Receptor α
TLDR
It is shown that PPARα is phosphorylated in response to stress stimuli in rat neonatal cardiac myocytes; in vitro kinase assays demonstrated that p38 MAPK phosphorylates serine residues located within the NH2-terminal A/B domain of the protein. Expand
Activation of cardiac Cdk9 represses PGC‐1 and confers a predisposition to heart failure
TLDR
It is reported that αMHC‐cyclin T1 mice appear normal at baseline yet suffer fulminant apoptotic cardiomyopathy when challenged by mechanical stress or signaling by the G‐protein Gq. Expand
PPAR signaling in the control of cardiac energy metabolism.
TLDR
PPARalpha not only serves a critical role in normal cardiac metabolic homeostasis, but alterations in PPARalpha signaling likely contribute to the pathogenesis of a variety of disease states. Expand
Necrotic Myocardial Cells Release Damage-Associated Molecular Patterns That Provoke Fibroblast Activation In Vitro and Trigger Myocardial Inflammation and Fibrosis In Vivo
TLDR
These studies constitute the initial demonstration that DAMPs released by NMCs induce fibroblast activation in vitro, as well as myocardial inflammation and fibrosis in vivo, at least in part, through TLR4-dependent signaling. Expand
Transcriptional control of a nuclear gene encoding a mitochondrial fatty acid oxidation enzyme in transgenic mice: role for nuclear receptors in cardiac and brown adipose expression
TLDR
An important role for nuclear receptors in the transcriptional control of a nuclear gene encoding a mitochondrial fatty acid oxidation enzyme is dictated and a gene regulatory pathway involved in cardiac energy metabolism is identified. Expand
The Development of Myocardial Fibrosis in Transgenic Mice With Targeted Overexpression of Tumor Necrosis Factor Requires Mast Cell–Fibroblast Interactions
TLDR
It is suggested that increased mast cell density with resultant mast cell–cardiac fibroblast cross-talk is required for the development of myocardial fibrosis in inflammatory cardiomyopathy. Expand
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