Abstract:
:Peroxisome proliferator-activated receptors (PPAR)alpha, gamma and beta/delta belong to the nuclear receptor family of ligand-activated transcription factors. PPARs heterodimerize with the retinoid X receptor (RXR) and then act as transcription factors to modulate the function of many target genes. PPARalpha, gamma and beta/delta subtypes have significant differences in their ligand and gene specificities. PPARalpha is activated by polyunsaturated fatty acids and by fibrate drugs (fenofibrate and gemfibrozil) and controls expression of genes involved in lipid metabolism. PPARgamma is activated by fatty acid derivatives, such as hydroxyoctadecadienoic acid (HODEs), prostaglandin derivatives, such as 15-deoxy-Delta12,14-prostaglandin J2, and thiazolidinedione (glitazone) drugs, such as pioglitazone and rosiglitazone. PPARgamma is a key regulator of glucose homeostasis and adipogenesis. PPARbeta/delta ligands include polyunsaturated fatty acids, prostaglandins and synthetic compounds and stimulate fatty acid oxidation. All PPARs are expressed in vascular cells where they exert antiatherogenic, anti-inflammatory and vasculoprotective actions. Activators of PPARalpha (fibrates) and PPARgamma (thiazolidinediones or glitazones) antagonize angiotensin II effects in vivo and in vitro and have cardiovascular antioxidant and anti-inflammatory actions. PPAR agonists slightly reduce blood pressure are cardio-protective and correct vascular structure and endothelial dysfunction in experimental models of hypertension. Because of these beneficial effects, activators of PPARs may have therapeutic potential in the prevention of cardiovascular disease beyond their actions on carbohydrate and lipid metabolism. The present chapter focuses on the role of PPARs in vascular biology and discusses the clinical implications of using PPAR agonists in the management of vascular disease.
journal_name
Vascul Pharmacoljournal_title
Vascular pharmacologyauthors
Touyz RM,Schiffrin ELdoi
10.1016/j.vph.2005.11.014subject
Has Abstractpub_date
2006-07-01 00:00:00pages
19-28issue
1eissn
1537-1891issn
1879-3649pii
S1537-1891(06)00082-6journal_volume
45pub_type
杂志文章,评审abstract::Increased TNFα-mediated JNK signaling in the perivascular adipose tissue (PVAT) may contribute to the pathogenesis of vascular complications in T1DM by reducing adiponectin (Ad) synthesis and therefore impairing Ad-mediated activity in the contiguous blood vessel system. We evaluated whether in vivo treatment with the...
journal_title:Vascular pharmacology
pub_type: 杂志文章
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abstract::Phosphorylation of proteins on tyrosine acts as a reversible and specific trigger mechanism, forming or disrupting regulatory connections between proteins. Tyrosine kinases and phosphatases participate in multiple cellular processes, and considerable evidence now supports a role for tyrosine phosphorylation in vascula...
journal_title:Vascular pharmacology
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doi:10.1016/s1537-1891(03)00009-0
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abstract::Endothelial cell dysfunction is considered to be an early event which subsequently leads to vascular wall disorders. Ultrastructural studies indicate that the endothelial cell changes involve membrane damage, increased permeability, swelling and necrosis. The endothelial cell loss of function could be as a result of c...
journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
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abstract::In systemic sclerosis, microvascular injury often precedes the development of fibrosis. Whereas the development of digital ulcers and skin fibrosis causes high morbidity, the affection of internal organs, in particular complications such as interstitial lung disease and pulmonary (arterial) hypertension, account for t...
journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2012.12.001
更新日期:2013-03-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 临床试验,杂志文章,随机对照试验
doi:10.1016/s1537-1891(02)00300-2
更新日期:2002-08-01 00:00:00
abstract::Unresolved endoplasmic reticulum (ER) stress, with the subsequent persistent activation of the unfolded protein response (UPR) is a well-recognized mechanism of endothelial cell apoptosis with a major impact on the integrity of the endothelium during the course of cardiovascular diseases. As in other cell types, Ca(2+...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2015.07.011
更新日期:2016-01-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2006.12.004
更新日期:2007-06-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2012.01.008
更新日期:2012-03-01 00:00:00
abstract::The purpose of this study was to determine if P-selectin, an adhesion molecule involved in the transendothelial movement of leukocytes, might also have a direct influence on the function of cells that come into contact with it. Human peripheral blood mononuclear cells were incubated on immobilized P-selectin or a cont...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2005.11.002
更新日期:2006-03-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章,meta分析,评审
doi:10.1016/j.vph.2015.09.005
更新日期:2016-05-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2012.08.007
更新日期:2013-01-01 00:00:00
abstract::Activation of ATP-sensitive K+ channels (K ATP) during ischemia leads to arrhythmias and blockade of these channels exert antiarrhythmic action. In this study, we investigated the effects of HMR1098, a sarcolemmal K ATP channel blocker and 5-hydroxydeconoate (5-HD), a mitochondrial K ATP channel blocker on cardiac fun...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2005.11.006
更新日期:2006-04-01 00:00:00
abstract::The antiplatelet and antithrombotic activities of a newly synthesized CP201, 2-(3,5-di-tert-butyl-4-hydroxyl)-3-chloro-1,4-naphthoquinone on human platelet aggregation in vitro and murine pulmonary thrombosis in vivo were examined. In addition, the antiplatelet activity of CP201 involved in calcium-signaling cascade w...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2004.04.001
更新日期:2004-02-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2016.05.015
更新日期:2016-09-01 00:00:00
abstract::AMP-activated protein kinase (AMPK) is present in the arterial wall and is activated in response to cellular stressors that raise AMP relative to ADP/ATP. Activation of AMPK in vivo lowers blood pressure but the influence of hyperlipidemia on this response has not been studied. ApoE(-/-) mice on high fat diet for 6wee...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2015.07.010
更新日期:2015-11-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2016.02.005
更新日期:2016-07-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2018.04.003
更新日期:2018-04-12 00:00:00
abstract::Evidence from both clinical and experimental studies indicates that Di-peptidyl peptidase-IV (DPP-4) inhibition may mediate favorable effects on the cardiovascular system. The objective of this study was to examine the acute effects of DPP-4 inhibition on vascular responses and to study the underlying mechanisms of al...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2011.03.001
更新日期:2011-07-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2006.10.011
更新日期:2007-04-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2012.11.004
更新日期:2013-04-01 00:00:00
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pub_type: 杂志文章
doi:10.1016/j.vph.2019.05.001
更新日期:2019-01-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2008.06.001
更新日期:2008-08-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2005.09.006
更新日期:2006-01-01 00:00:00
abstract::Bemiparin is a low molecular weight heparin (LMWH) indicated for the acute treatment of deep vein thrombosis with or without pulmonary embolism, for the prophylaxis of venous thromboembolism in surgical and non-surgical patients and for the prevention of clotting in the extracorporeal circuit during hemodialysis. Due ...
journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2014.03.001
更新日期:2014-07-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2014.03.008
更新日期:2014-05-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2015.05.015
更新日期:2015-08-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2003.09.002
更新日期:2003-12-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2005.04.003
更新日期:2005-08-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2005.02.012
更新日期:2005-08-01 00:00:00
abstract::The A3 adenosine receptor (A3AR) is attributed with multiple beneficial actions in ischemic-reperfused myocardium, including modulation of oncotic and apoptotic cell death and enhancement of contractile function. Additionally, the A3AR may attenuate vascular dysfunction and improve long-term outcome from myocardial in...
journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2005.02.009
更新日期:2005-04-01 00:00:00