Peroxisome proliferator-activated receptor delta and cardiovascular disease

Skogsberg, Josefin

doi:10.1016/j.atherosclerosis.2013.08.027

Cited by 32 publications

(41 citation statements)

References 108 publications

(186 reference statements)

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“…In a number of studies, atherosclerosis was induced by collar placement, electric and balloon injury/denudation (Ameli et al, 1994;Chiesa, 2002;Corti et al, 2007;Ibanez et al, 2012;Ibanez et al, 2008;Nicholls et al, 2005;Parolini et al, 2008;Soma et al, 1995). The effects of PPAR-δ agonists (Ehrenborg and Skogsberg, 2013) and miR-33 antagonism (Hennessy and Moore, 2013) on atherosclerosis development were investigated in animals that do not express CETP and according to or knowledge have not been tested in an animal model with a more human-like lipoprotein metabolism. Studies of LXR and FXR agonists in CETPexpressing animals were not included in this review, since no increase in HDL-C was observed except for the study by Srivastava et al evaluating the anti-atherosclerotic activities of PPAR-α, PPAR-γ and LXR agonist (T0901317) in F1B hamsters (Srivastava, 2011).…”

Section: Study Design and Baseline Lipid Levelsmentioning

confidence: 98%

Innovative pharmaceutical interventions in cardiovascular disease: Focusing on the contribution of non-HDL-C/LDL-C-lowering versus HDL-C-raisingA systematic review and meta-analysis of relevant preclinical studies and clinical trials

Kühnast

Fiocco

Hoorn

et al. 2015

European Journal of Pharmacology

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Section: Study Design and Baseline Lipid Levelsmentioning

confidence: 98%

Innovative pharmaceutical interventions in cardiovascular disease: Focusing on the contribution of non-HDL-C/LDL-C-lowering versus HDL-C-raisingA systematic review and meta-analysis of relevant preclinical studies and clinical trials

Kühnast

Fiocco

Hoorn

et al. 2015

European Journal of Pharmacology

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“…PPARD is distributed in nearly every part of the body (Dongiovanni and Valenti, 2013). PPARD plays a key role in the regulation of multiple important biological processes, including lipid metabolism, insulin sensitivity, and atherosclerosis formation (Ehrenborg and Skogsberg, 2013). PPARD agonists can increase the levels of plasma high-density lipoprotein cholesterol (HDL-C) (Oliver et al, 2001), HDL-C is known to protect CHD in humans (Wilson et al, 1980).…”

Section: Introductionmentioning

confidence: 99%

Positive association between PPARD rs2016520 polymorphism and coronary heart disease in a Han Chinese population

Ye¹,

Li²,

Hong³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. PPARD encodes peroxisome proliferator-activated receptor delta, which has been shown to play an important role in controlling lipid metabolism and atherosclerosis. In this case-control study, we explored the relationship between PPARD rs2016520 polymorphism and coronary heart disease (CHD) in a Han Chinese population. A total of 657 CHD cases and 640 controls were included in the association study. rs2016520 polymorphism genotyping was performed using the melting temperature-shift polymerase chain reaction method. The PPARD rs2016520-G allele reduced CHD risk by 17.9% (χ 2 = 5.061, In contrast, meta-analysis of PPARD rs2016520 among 3732 cases and 5042 controls revealed no association between PPARD rs2016520 and CHD (P = 0.19). We found that the PPARD rs2016520-GG genotype decreased CHD risk in a Han Chinese population. Moreover, we found an association between serum highdensity lipoprotein cholesterol level and PPARD rs2016520 in senior individuals aged ≥ 65 years. The meta-analysis revealed no association between PPARD rs2016520 and CHD, suggesting ethnic differences in the association between the PPARD locus and CHD.

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“…30 Prior studies suggest that systemic activation of PPARd is protective against major cardiovascular risk factors including dyslipidemia, insulin resistance, and obesity. 30 In peripheral blood vessels, pharmacological analysis demonstrated that PPARd agonists exert vascular protective effects 13,31,32 ; however, the role of PPARd in cerebral vascular function is not fully understood. In our previous study we demonstrated that in the cerebral microvessels, activation of PPARd prevented endothelial dysfunction thereby suggesting that endothelial PPARd might be an important vasoprotective molecule.…”

mentioning

confidence: 99%

mentioning

confidence: 99%

“…30 Besides their role in the control of metabolism, PPAR isoforms are essential regulators of cardiovascular system. 30 Prior studies suggest that systemic activation of PPARd is protective against major cardiovascular risk factors including dyslipidemia, insulin resistance, and obesity. 30 In peripheral blood vessels, pharmacological analysis demonstrated that PPARd agonists exert vascular protective effects 13,31,32 ; however, the role of PPARd in cerebral vascular function is not fully understood.…”

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confidence: 99%

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Role of prostacyclin signaling in endothelial production of soluble amyloid precursor protein-α in cerebral microvessels

Santhanam

Lü

et al. 2016

J Cereb Blood Flow Metab

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We tested hypothesis that activation of the prostacyclin (PGI 2 ) receptor (IP receptor) signaling pathway in cerebral microvessels plays an important role in the metabolism of amyloid precursor protein (APP). In human brain microvascular endothelial cells activation of IP receptor with the stable analogue of PGI 2 , iloprost, stimulated expression of amyloid precursor protein and a disintegrin and metalloprotease 10 (ADAM10), resulting in an increased production of the neuroprotective and anticoagulant molecule, soluble APPa (sAPPa). Selective agonist of IP receptor, cicaprost, and adenylyl cyclase activator, forskolin, also enhanced expression of amyloid precursor protein and ADAM10. Notably, in cerebral microvessels of IP receptor knockout mice, protein levels of APP and ADAM10 were reduced. In addition, iloprost increased protein levels of peroxisome proliferator-activated receptor d (PPARd) in human brain microvascular endothelial cells. PPARd-siRNA abolished iloprost-augmented protein expression of ADAM10. In contrast, GW501516 (a selective agonist of PPARd) upregulated ADAM10 and increased production of sAPPa. Genetic deletion of endothelial PPARd (ePPARd À/À ) in mice significantly reduced cerebral microvascular expression of ADAM10 and production of sAPPa. In vivo treatment with GW501516 increased sAPPa content in hippocampus of wild type mice but not in hippocampus of ePPARd À/À mice. Our findings identified previously unrecognized role of IP-PPARd signal transduction pathway in the production of sAPPa in cerebral microvasculature.

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Peroxisome proliferator-activated receptor delta and cardiovascular disease

Cited by 32 publications

References 108 publications

Innovative pharmaceutical interventions in cardiovascular disease: Focusing on the contribution of non-HDL-C/LDL-C-lowering versus HDL-C-raisingA systematic review and meta-analysis of relevant preclinical studies and clinical trials

Innovative pharmaceutical interventions in cardiovascular disease: Focusing on the contribution of non-HDL-C/LDL-C-lowering versus HDL-C-raisingA systematic review and meta-analysis of relevant preclinical studies and clinical trials

Positive association between PPARD rs2016520 polymorphism and coronary heart disease in a Han Chinese population

Role of prostacyclin signaling in endothelial production of soluble amyloid precursor protein-α in cerebral microvessels

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