scholarly journals Protecting against vascular disease in brain

2011 ◽  
Vol 300 (5) ◽  
pp. H1566-H1582 ◽  
Author(s):  
Frank M. Faraci
Keyword(s):  
Vascular Disease ◽  
Renin Angiotensin System ◽  
Peroxisome Proliferator ◽  
Vascular Protection ◽  
Peroxisome Proliferator Activated Receptor ◽  
Angiotensin System ◽  
New Concepts ◽  
Vascular Component ◽  
Inflammatory Molecules

Endothelial cells exert an enormous influence on blood vessels throughout the circulation, but their impact is particularly pronounced in the brain. New concepts have emerged recently regarding the role of this cell type and mechanisms that contribute to endothelial dysfunction and vascular disease. Activation of the renin-angiotensin system plays a prominent role in producing these abnormalities. Both oxidative stress and local inflammation are key mechanisms that underlie vascular disease of diverse etiology. Endogenous mechanisms of vascular protection are also present, including antioxidants, anti-inflammatory molecules, and peroxisome proliferator-activated receptor-γ. Despite their clear importance, studies of mechanisms that underlie cerebrovascular disease continue to lag behind studies of vascular biology in general. Identification of endogenous molecules and pathways that protect the vasculature may result in targeted approaches to prevent or slow the progression of vascular disease that causes stroke and contributes to the vascular component of dementia and Alzheimer's disease.

scholarly journals Young Investigator Award Lecture of the APS Water and Electrolyte Homeostasis Section, 2008: The pathophysiology of hypertension in systemic lupus erythematosus

2009 ◽  
Vol 296 (4) ◽  
pp. R1258-R1267 ◽  
Author(s):  
Michael J. Ryan
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Cardiovascular Disease ◽  
Chronic Inflammation ◽  
Lupus Erythematosus ◽  
Renin Angiotensin System ◽  
Peroxisome Proliferator ◽  
Inflammatory Disorder ◽  
Systemic Lupus ◽  
Peroxisome Proliferator Activated Receptor

Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disorder that predominantly affects women during their reproductive years. Although SLE can affect any organ system, the kidneys are prominently involved in the form of immune complex glomerulonephritis. In addition, in women with SLE, risk for the development of cardiovascular disease is dramatically increased. Hypertension is a major risk factor for cardiovascular disease and is highly prevalent in women with SLE. Nevertheless, there has been little exploration of the pathophysiological mechanisms that promote SLE hypertension. This review discusses the role of several mechanisms, with an emphasis on the kidney, in SLE hypertension. These mechanisms include the renin-angiotensin system, endothelin, oxidative stress, sex steroids, metabolic changes, peroxisome proliferator-activated receptor-γ, and, perhaps most importantly, chronic inflammation and cytokines. Growing evidence suggests a link between chronic inflammation and hypertension. Therefore, elucidation of mechanisms that promote SLE hypertension may be of significant value not only for patients with SLE, but also for a better understanding of the basis for essential hypertension.

scholarly journals The Role of PPARγ in Cardiovascular Diseases

2016 ◽  
pp. S343-S363 ◽  
Author(s):  
M. KVANDOVÁ ◽  
M. MAJZÚNOVÁ ◽  
I. DOVINOVÁ
Keyword(s):  
Insulin Signaling ◽  
Renin Angiotensin System ◽  
Oxidative Stress Response ◽  
Peroxisome Proliferator ◽  
Pressure Regulation ◽  
Angiotensin System ◽  
Nrf2 Activation ◽  
Peroxisome Proliferator Activated Receptors ◽  
Progression Of Atherosclerosis

The peroxisome proliferator-activated receptors (PPAR) belong to the nuclear superfamily of ligand-activated transcription factors. PPARγ acts as a nutrient sensor that regulates several homeostatic functions. Its disruption can lead to vascular pathologies, disorders of fatty acid/lipid metabolism and insulin resistance. PPARγ can modulate several signaling pathways connected with blood pressure regulation. Firstly, it affects the insulin signaling pathway and endothelial dysfunction by modulation of expression and/or phosphorylation of signaling molecules through the PI3K/Akt/eNOS or MAPK/ET-1 pathways. Secondly, it can modulate gene expression of the renin- angiotensin system – cascade proteins, which potentially slow down the progression of atherosclerosis and hypertension. Thirdly, it can modulate oxidative stress response either directly through PPAR or indirectly through Nrf2 activation. In this context, activation and functioning of PPARγ is very important in the regulation of several disorders such as diabetes mellitus, hypertension and/or metabolic syndrome.

scholarly journals Sex-dependent effects of antenatal glucocorticoids on insulin sensitivity in adult sheep: role of the adipose tissue renin angiotensin system

2017 ◽  
Vol 312 (6) ◽  
pp. R1029-R1038 ◽  
Author(s):  
G. Angela Massmann ◽  
Jie Zhang ◽  
Won Joon Seong ◽  
Minhyoung Kim ◽  
Jorge P. Figueroa
Keyword(s):  
Adipose Tissue ◽  
Glucose Tolerance ◽  
Mrna Expression ◽  
Renin Angiotensin System ◽  
Female Offspring ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ppar Γ ◽  
Pregnant Sheep

Exposure to glucocorticoids in utero is associated with changes in organ function and structure in the adult. The aims of this study were to characterize the effects of antenatal exposure to glucocorticoids on glucose handling and the role of adipose tissue. Pregnant sheep received betamethasone (Beta, 0.17 mg/kg) or vehicle 24 h apart at 80 days of gestation and allowed to deliver at term. At 9 mo, male and female offspring were fed at either 100% of nutritional allowance (lean) or ad libitum for 3 mo (obese). At 1 yr, they were chronically instrumented under general anesthesia. Glucose tolerance was evaluated using a bolus of glucose (0.25 g/kg). Adipose tissue was harvested after death to determine mRNA expression levels of angiotensinogen (AGT), angiotensin-converting enzyme (ACE) 1, ACE2, and peroxisome proliferator-activated receptor γ (PPAR-γ). Data are expressed as means ± SE and analyzed by ANOVA. Sex, obesity, and Beta exposure had significant effects on glucose tolerance and mRNA expression. Beta impaired glucose tolerance in lean females but not males. Superimposed obesity worsened the impairment in females and unmasked the defect in males. Beta increased ACE1 mRNA in females and males and AGT in females only ( P < 0.05 by three-way ANOVA). Obesity increased AGT in females but had no effect on ACE1 in either males or females. PPAR-γ mRNA exhibited a significant sex ( F = 42.8; P < 0.01) and obesity ( F = 6.9; P < 0.05) effect and was significantly higher in males ( P < 0.01 by three-way ANOVA). We conclude that adipose tissue may play an important role in the sexually dimorphic response to antenatal glucocorticoids.

scholarly journals New Concepts in Malaria Pathogenesis: The Role of the Renin-Angiotensin System

2016 ◽  
Vol 5 ◽  
Author(s):  
Leandro S. Silva ◽  
João Luiz Silva-Filho ◽  
Celso Caruso-Neves ◽  
Ana Acacia S. Pinheiro
Keyword(s):  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
New Concepts

scholarly journals PPARγin Kidney Physiology and Pathophysiology

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-9 ◽  
Author(s):  
Éva Kiss-Tóth ◽  
Tamás Rőszer
Keyword(s):  
Kidney Development ◽  
Current Knowledge ◽  
Renin Angiotensin System ◽  
Common Side Effect ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Angiotensin System ◽  
Beneficial Effects ◽  
Kidney Physiology ◽  
Interstitial Fluid Volume

Involvement of the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ) in kidney physiology has been explored recently. Synthetic PPARγligands can ameliorate the diabetic kidney disease through different mechanisms, involving inhibition of mesangial cell growth, reduction of mesangial matrix, and cytokine production of glomerular cells as well as promoting endothelial cell survival within the kidney glomeruli. Activation of PPARγhas additional profibrotic consequences, which can contribute to wound healing in diabetic glomerulonephritis. Beside many beneficial effects, PPARγactivation, however, can lead to severe water retention, a common side effect of thiazolidinedione therapy. This unwanted effect is due to the activation of PPARγin the mesonephric distal collecting system, where PPARγpositively regulates sodium and water resorbtion leading to the expansion of interstitial fluid volume. Recent studies indicate that PPARγis also involved in the normal kidney development, renal lipid metabolism, and activation of the renin-angiotensin system. In this paper, we give a synopsis of the current knowledge on PPARγfunctions in kidney phyisology and pathophysiology.

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