Dysfonctionnement cardiaque secondaire à un orage adrénergique ou cardiomyopathie de stress chez l’enfant victime d’un traumatisme

Batouche, D.D.; Elhalimi, K.; Benatta, N.F.

doi:10.1016/j.ancard.2016.04.022

Cited by 3 publications

(3 citation statements)

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“…As indicated earlier, several studies have shown that PPAR gamma and the Wnt/beta-catenin pathway operate through an antagonistic manner (Gerhold et al, 2002 ; Moldes et al, 2003 ; Sharma et al, 2004 ; Garcia-Gras et al, 2006 ; Liu et al, 2006 ; Takada et al, 2009 ; Lu and Carson, 2010 ). Other diseases present a similar profile in terms of Wnt/beta-catenin /PPAR gamma signaling, i.e., ARVC, osteoporosis, cardiac hypertrophy, bipolar disorder, and schizophrenia (Lecarpentier et al, 2014 ). Thus, the high PPAR gamma levels observed in AD may contribute to inhibit the Wnt/beta-catenin pathway (Figure 2 ).…”

Section: Alzheimer's Disease (Ad) Generalitiesmentioning

confidence: 99%

“…PPAR alpha plays a pivotal role in lipid metabolism and anti-inflammatory processes. In many diseases, the expression of PPAR alpha generally varies inversely with that of PPAR gamma (Lecarpentier et al, 2014 ). Thus, in ARVD and cardiac hypertrophy, expression of PPAR gamma is high and expression of PPAR alpha is low, whereas the reverse has been observed in type 2 diabetes and hypertension (Finck et al, 2002 ; Feige et al, 2006 ; Djouadi et al, 2009 ).…”

Section: Alzheimer's Disease (Ad) Generalitiesmentioning

confidence: 99%

“…The AD pathophysiology is not completely understood but is characterized by the deposition of extracellular Abeta plaques (Abeta) and the formation of intracellular neurofibrillary tangles (NFTs) in the central nervous system (CNS) (Mattson, 2004 ; Mayeux and Stern, 2012 ). Certain neurodegenerative diseases (NDs) have recently been classified into two categories (Lecarpentier et al, 2014 ). Amyotrophic lateral sclerosis (Lecarpentier and Vallee, 2016 ), Parkinson's disease, Huntington's disease, multiple sclerosis and Friedreich's ataxia represent NDs in which the canonical Wnt/beta-catenin pathway is upregulated while PPAR gamma is downregulated.…”

Section: Introductionmentioning

confidence: 99%

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Alzheimer Disease: Crosstalk between the Canonical Wnt/Beta-Catenin Pathway and PPARs Alpha and Gamma

Vallée¹,

Lecarpentier²

2016

Front. Neurosci.

115

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The molecular mechanisms underlying the pathophysiology of Alzheimer's disease (AD) are still not fully understood. In AD, Wnt/beta-catenin signaling has been shown to be downregulated while the peroxisome proliferator-activated receptor (PPAR) gamma (mARN and protein) is upregulated. Certain neurodegenerative diseases share the same Wnt/beta-catenin/PPAR gamma profile, such as bipolar disorder and schizophrenia. Conversely, other NDs share an opposite profile, such as amyotrophic lateral sclerosis, Parkinson's disease, Huntington's disease, multiple sclerosis, and Friedreich's ataxia. AD is characterized by the deposition of extracellular Abeta plaques and the formation of intracellular neurofibrillary tangles in the central nervous system (CNS). Activation of Wnt signaling or inhibition of both glycogen synthase kinase-3beta and Dickkopf 1, two key negative regulators of the canonical Wnt pathway, are able to protect against Abeta neurotoxicity and to ameliorate cognitive performance in AD patients. Although PPAR gamma is upregulated in AD patients, and despite the fact that it has been shown that the PPAR gamma and Wnt/beta catenin pathway systems work in an opposite manner, PPAR gamma agonists diminish learning and memory deficits, decrease Abeta activation of microglia, and prevent hippocampal and cortical neurons from dying. These beneficial effects observed in AD transgenic mice and patients might be partially due to the anti-inflammatory properties of PPAR gamma agonists. Moreover, activation of PPAR alpha upregulates transcription of the alpha-secretase gene and represents a new therapeutic treatment for AD. This review focuses largely on the behavior of two opposing pathways in AD, namely Wnt/beta-catenin signaling and PPAR gamma. It is hoped that this approach may help to develop novel AD therapeutic strategies integrating PPAR alpha signaling.

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