Zobrazeno 1 - 10
of 30
pro vyhledávání: '"Quy N. Diep"'
Publikováno v:
Canadian Journal of Physiology and Pharmacology. 83:999-1006
Activation of the renin–angiotensin–aldosterone system is associated with increased extracellular matrix and inflammatory markers in the cardiovascular system. We evaluated the effects of aldosterone antagonism on cardiovascular structure, collag
Publikováno v:
Canadian Journal of Physiology and Pharmacology. 82:976-985
We investigated the long-term effects of the thiazolidinedione PPARγ activator pioglitazone on cardiac inflammation in stroke-prone spontaneously hypertensive rats (SHRSP), a model of malignant of hypertension. Six-week-old SHRSP were treated with p
Autor:
Dierk Endemann, Jeffrey S. Cohn, Karim Benkirane, Farhad Amiri, Quy N. Diep, Ernesto L. Schiffrin
Publikováno v:
Journal of Molecular and Cellular Cardiology. 36:295-304
Peroxisome proliferator-activated receptor (PPAR)alpha is highly expressed in the heart. PPAR alpha may play a role in cardiac hypertrophy, but effects on cardiac function, inflammation, and fibrosis are unknown. We tested the hypothesis that the PPA
Publikováno v:
Hypertension. 42:664-668
Peroxisome proliferator-activated receptors (PPAR) are nuclear receptors acting as transcription factors on numerous target genes after heterodimerization with the retinoid X receptor. PPAR-α and PPAR-γ may be activated by different agonists, altho
Autor:
Marc Iglarz, Rhian M. Touyz, Marie-France Lavoie, Ernesto L. Schiffrin, Quy N. Diep, Farhad Amiri
Publikováno v:
Arteriosclerosis, Thrombosis, and Vascular Biology. 23:45-51
Objective— Peroxisome proliferator–activated receptors (PPARs) may modulate in vitro the vascular production of vasoactive peptides such as endothelin-1 (ET-1). Thus, we investigated in vivo the interaction between PPARs and ET-1 in deoxycorticos
Autor:
Ernesto L. Schiffrin, Quy N. Diep
Publikováno v:
Hypertension. 38:249-254
Peroxisome proliferator-activated receptors (PPARs) are a family of ligand-activated transcription factors that include PPAR-α, PPAR-γ, and PPAR-δ. We hypothesized that PPAR expression in blood vessels could be reduced in hypertension to result in
Publikováno v:
Hypertension. 37:604-608
Angiotensin II is an important modulator of cell growth through AT 1 receptors, as demonstrated both in vivo and in vitro. We investigated the role of proteins involved in the cell cycle, including cyclin D1, cyclin-dependent kinase 4 (cdk4), and cyc
Publikováno v:
Hypertension. 36:851-855
Abstract —Omega-3 fatty acids (n-3 FAs) have been shown to exert a blood pressure–lowering effect in hypertension, possibly in part by influencing vascular structure. We previously demonstrated that n-3 FAs induce vascular smooth muscle cell (VSM
Publikováno v:
Hypertension. 35:287-291
Abstract —Endothelin-1 (ET-1) may be involved in the induction of vascular hypertrophy in hypertension. ET-1 may also modulate vascular growth through the exertion of antiapoptotic effects. The ω3 fatty acids (ω3 FAs), which have antiproliferativ
Publikováno v:
Hypertension. 34:617-624
Abstract —In vitro experiments suggest that angiotensin II (Ang II) may cause growth via angiotensin type 1 (AT 1 ) receptors and apoptosis via angiotensin type 2 (AT 2 ) receptors. To answer the question of whether AT 1 or AT 2 receptor activation