Cardiac hypertrophy is enhanced in PPAR -/- mice in response to chronic pressure overload (Q57244167)

1

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B. E.J. Teunissen

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P. H.M. Willemsen

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F. A. van Nieuwenhoven

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A. E. Brouns

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B. J.A. Janssen

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J. P.M. Cleutjens

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G. J. van der Vusse

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M. van Bilsen

Cardiac hypertrophy: the good, the bad, and the ugly

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publication date

10 January 2008

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published in

Cardiovascular Research

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volume

78

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issue

1

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page(s)

79-89

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cites work

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Controversies in ventricular remodelling

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Tumor necrosis factor alpha induces human atrial myofibroblast proliferation, invasion and MMP-9 secretion: inhibition by simvastatin

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IL-1beta and TNF-alpha upregulate angiotensin II type 1 (AT1) receptors on cardiac fibroblasts and are associated with increased AT1 density in the post-MI heart

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Inhibition of NF-kappaB induces regression of cardiac hypertrophy, independent of blood pressure control, in spontaneously hypertensive rats

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PPAR alpha activator fenofibrate inhibits myocardial inflammation and fibrosis in angiotensin II-infused rats

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Activation of PPARdelta inhibits cardiac fibroblast proliferation and the transdifferentiation into myofibroblasts.

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Altered Constitutive Expression of Fatty Acid-metabolizing Enzymes in Mice Lacking the Peroxisome Proliferator-activated Receptor α (PPARα)

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A critical role for the peroxisome proliferator-activated receptor alpha (PPARalpha) in the cellular fasting response: the PPARalpha-null mouse as a model of fatty acid oxidation disorders

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Fatty acid homeostasis and induction of lipid regulatory genes in skeletal muscles of peroxisome proliferator-activated receptor (PPAR) alpha knock-out mice. Evidence for compensatory regulation by PPAR delta

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Decreased contractile and metabolic reserve in peroxisome proliferator-activated receptor-alpha-null hearts can be rescued by increasing glucose transport and utilization

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PPAR-alpha activation required for decreased glucose uptake and increased susceptibility to injury during ischemia

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A critical role for peroxisomal proliferator-activated receptor-alpha nuclear receptors in the development of cardiomyocyte degeneration and necrosis

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Expression of heme oxygenase-1 in human vascular cells is regulated by peroxisome proliferator-activated receptors

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Endothelin-1-induced cardiac hypertrophy is inhibited by activation of peroxisome proliferator-activated receptor-alpha partly via blockade of c-Jun NH2-terminal kinase pathway

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Peroxisome proliferator activated receptor (PPAR)alpha agonists inhibit hypertrophy of neonatal rat cardiac myocytes

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Peroxisome proliferator-activated receptor alpha-independent actions of fenofibrate exacerbates left ventricular dilation and fibrosis in chronic pressure overload.

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Cardiac fatty acid metabolism is preserved in the compensated hypertrophic rat heart

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NF-kappaB activation is required for the development of cardiac hypertrophy in vivo

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Activation of NF-kappa B is required for hypertrophic growth of primary rat neonatal ventricular cardiomyocytes

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Role of oxidative stress in cardiac dysfunction of PPARα−/− mice

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