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Endothelium-Restricted Overexpression of Human Endothelin-1 Causes Vascular Remodeling and Endothelial Dysfunction
TLDR
In this new murine model of endothelium-restricted human preproET-1 overexpression, ET-1 caused structural remodeling and endothelial dysfunction of resistance vessels, consistent with a direct nonhemodynamic effect of ET- 1 on the vasculature, at least in part through the activation of vascular NAD(P)H oxidase. Expand
Spironolactone Improves Angiotensin-Induced Vascular Changes and Oxidative Stress
TLDR
Spironolactone, which inhibited aldosterone actions, partially corrected structural and functional angiotensin II–induced abnormalities and was associated with reduced vascular NADPH oxidase activity and decreased plasma markers of oxidative stress. Expand
Angiotensin II and endothelin-1 regulate MAP kinases through different redox-dependent mechanisms in human vascular smooth muscle cells
TLDR
The data suggest that redox-dependent activation of MAPKs by Ang II and ET-1 occur through distinct ROS-generating systems that could contribute to differential signaling by these agonists in VSMCs. Expand
Role of NAD(P)H oxidase on vascular alterations in angiotensin II-infused mice
TLDR
The findings suggest that NAD(P)H oxidase activity plays an important role in vascular functional and structural changes and in the composition of the vascular wall in Ang II-dependent hypertension. Expand
Reduced Vascular Remodeling, Endothelial Dysfunction, and Oxidative Stress in Resistance Arteries of Angiotensin II–Infused Macrophage Colony-Stimulating Factor–Deficient Mice: Evidence for a Role in
TLDR
m-CSF–deficient mice (Op/Op) developed less endothelial dysfunction, vascular remodeling, and oxidative stress induced by Ang II than +/+ littermates, suggesting a critical role of m- CSF and proinflammatory mediators in Ang II-induced vascular injury. Expand
Structure, Endothelial Function, Cell Growth, and Inflammation in Blood Vessels of Angiotensin II–Infused Rats: Role of Peroxisome Proliferator–Activated Receptor-&ggr;
TLDR
Thiazolidinedione PPAR-&ggr; activators attenuated the development of hypertension, corrected structural abnormalities, normalized cell growth, and improved endothelial dysfunction induced by Ang II and prevented upregulation of angiotensin II type 1 receptors, cell cycle proteins, and proinflammatory mediators. Expand
Inhibition of the Jak/STAT signaling pathway prevents the high glucose-induced increase in tgf-beta and fibronectin synthesis in mesangial cells.
TLDR
Results provide direct evidence for linkages between JAK2, STAT1, and the glucose-induced overproduction of TGF-beta and fibronectin in GMC. Expand
Angiotensin II activation of the JAK/STAT pathway in mesangial cells is altered by high glucose.
TLDR
Evidence is provided that activation of the JAK/STAT pathway by HG or/and Ang II may be of importance in the increased GMC cell growth and collagen IV synthesis that is seen in diabetic nephropathy. Expand
Angiotensin II blockade prevents hyperglycemia-induced activation of JAK and STAT proteins in diabetic rat kidney glomeruli.
TLDR
It is demonstrated that hyperglycemia induces activation of JAK2 and the STATs in vivo via an ANG II-dependent mechanism and that these proteins may be involved in the early kidney damage associated with diabetes. Expand
PPAR alpha activator fenofibrate inhibits myocardial inflammation and fibrosis in angiotensin II-infused rats.
TLDR
The hypolipidemic drug fenofibrate may be useful in prevention and treatment of myocardial disease associated with hypertension and hyperlipidemia and its effects on cardiac function, inflammation, and fibrosis are unknown. Expand
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