Gene/Protein Disease Symptom Drug Enzyme Compound
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Diabetics are subjects to a high cardiovascular risk. This concept is now accepted by all and has been demonstrated in clinical practice by the constantly increasing number of diabetic cardiac patients and cardiac diabetics. The many therapeutic trials carried out on the prevention of cardiovascular complications in diabetics have made it possible to define therapeutic goals. HbA1c must be less than 6.5%. Target blood pressure values are 130/80 mmHg or even 125/75 in the case of renal insufficiency. If conventional treatments have proven efficacy against stroke and coronary events, only molecules which modulate the renin-angiotensin-aldosterone system provide additional nephroprotection in diabetics. However, single-agent therapy is seldom sufficient to achieve glycaemic or blood pressure targets. Diabetic dyslipidemia also requires attentive management, usually by a statin, with a target LDL cholesterol < 1 g/l at the onset of microalbuminuria. All these measures should make it possible to obtain a significant reduction in the cardiovascular risk of diabetic patients.
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PMID:[Diabetes and heart]. 1737 35

The metabolic syndrome is a cluster of common pathologies: abdominal obesity linked to an excess of visceral fat, insulin resistance, dyslipidemia and hypertension. This syndrome is occurring at epidemic rates, with dramatic consequences for human health worldwide, and appears to have emerged largely from changes in our diet and reduced physical activity. An important but not well-appreciated dietary change has been the substantial increase in fructose intake, which appears to be an important causative factor in the metabolic syndrome. There is also experimental and clinical evidence that the amount of magnesium in the western diet is insufficient to meet individual needs and that magnesium deficiency may contribute to insulin resistance. In recent years, several studies have been published that implicate subclinical chronic inflammation as an important pathogenic factor in the development of metabolic syndrome. Pro-inflammatory molecules produced by adipose tissue have been implicated in the development of insulin resistance. The present review will discuss experimental evidence showing that the metabolic syndrome, high fructose intake and low magnesium diet may all be linked to the inflammatory response. In many ways, fructose-fed rats display the changes observed in the metabolic syndrome and recent studies indicate that high-fructose feeding is associated with NADPH oxidase and renin-angiotensin activation. The production of reactive oxygen species results in the initiation and development of insulin resistance, hyperlipemia and high blood pressure in this model. In this rat model, a few days of experimental magnesium deficiency produces a clinical inflammatory syndrome characterized by leukocyte and macrophage activation, release of inflammatory cytokines, appearance of the acute phase proteins and excessive production of free radicals. Because magnesium acts as a natural calcium antagonist, the molecular basis for the inflammatory response is probably the result of a modulation of the intracellular calcium concentration. Potential mechanisms include the priming of phagocytic cells, the opening of calcium channels, activation of N-methyl-D-aspartate (NMDA) receptors, the activation of nuclear factor-kappaB (NFkB) and activation of the renin-angiotensin system. Since magnesium deficiency has a pro-inflammatory effect, the expected consequence would be an increased risk of developing insulin resistance when magnesium deficiency is combined with a high-fructose diet. Accordingly, magnesium deficiency combined with a high-fructose diet induces insulin resistance, hypertension, dyslipidemia, endothelial activation and prothrombic changes in combination with the upregulation of markers of inflammation and oxidative stress.
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PMID:High fructose consumption combined with low dietary magnesium intake may increase the incidence of the metabolic syndrome by inducing inflammation. 1740 91

In diabetic and nondiabetic chronic nephropathies, high blood pressure and urinary loss of proteins represent major determinants of progressive renal function decline. Reducing blood pressure with drugs that inhibit the renin-angiotensin system also lowers glomerular hypertension and ameliorates glomerular sieving properties, thus reducing proteinuria. Reducing urinary protein levels with angiotensin-converting enzyme inhibitors (ACEi) or angiotensin II receptor antagonists (ARA) limits renal function decline to the point that remission of disease and regression of renal lesions have been observed in experimental animals and in humans. This therapy, however, may not be effective in all patients. For patients who do not achieve complete remission of proteinuria, renoprotective treatment should include intensified blood pressure control (and metabolic control in diabetes) and amelioration of dyslipidemia. Early intervention, before progressive glomerulosclerosis and scarring is initiated by increased protein traffic, may be important to maximize reno- and cardioprotection, especially in diabetes.
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PMID:Does remission of renal disease associated with antihypertensive treatment exist? 1744 29

The course of diabetic nephropathy is affected by several factors that can be manipulated. In primary prevention, near normal metabolic control beginning at the time of the diagnosis of diabetes diminishes the risk of microalbuminuria to an extent depending on the HbA1c level attained. Hypertensive diabetics should be consistently treated with renin-angiotensin system (RAS)-blocking agents. In secondary prevention, a multifactorial therapy is able to stop or retard further progression. Its components are a sustained decrease of blood pressure in the normotensive range using RAS-blocking agents (normotensive patients should also be treated) as well as near normal metabolic control that takes into account the changing pharmacokinetic and pharmacodynamic properties of blood glucose-lowering drugs in renal insufficiency. Consideration of further factors (smoking, protein intake, anemia) and several general nephroprotective measures complete the treatment spectrum. Therapy for dyslipidemia and the administration of aspirin are important in view of the high cardiovascular morbidity. It is essential to monitor kidney function and the therapeutic components at short intervals.
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PMID:[Protection of renal function in diabetics]. 1757 24

Diabetes mellitus is as much a vascular disease as it is a metabolic disorder. The metabolic abnormalities associated with diabetes include hyperglycemia, and abnormal carbohydrate, fat, and protein handling. These abnormalities increase oxidative stress and activate the renin angiotensin system, which subsequently causes endothelial dysfunction and predisposes to atherosclerosis. Type 2 diabetes has reached epidemic proportions and because of its strong association with coronary artery disease (CAD), it is responsible for increasing cardiovascular morbidity and mortality in the United States. In this article we review some of the evidence and the rationale for comprehensive risk reduction to prevent and treat CAD in individuals with diabetes mellitus. The comprehensive risk reduction strategy includes lifestyle changes, glycemic control, and control of dyslipidemia and hypertension. Advances in revascularization techniques, and superior outcomes of coronary artery bypass grafting as an interventional modality over percutaneous coronary intervention, are discussed. We also identify controversies and issues that currently remain unresolved.
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PMID:Management of coronary artery disease in patients with type 2 diabetes mellitus. 1760 92

Accelerated cardiovascular disease is a frequent complication of renal disease. Chronic kidney disease promotes hypertension and dyslipidemia, which in turn can contribute to the progression of renal failure. Furthermore, diabetic nephropathy is the leading cause of renal failure in developed countries. Together, hypertension, dyslipidemia, and diabetes are major risk factors for the development of endothelial dysfunction and progression of atherosclerosis. Inflammatory mediators are often elevated and the renin-angiotensin system is frequently activated in chronic kidney disease, which likely contributes through enhanced production of reactive oxygen species to the accelerated atherosclerosis observed in chronic kidney disease. Promoters of calcification are increased and inhibitors of calcification are reduced, which favors metastatic vascular calcification, an important participant in vascular injury associated with end-stage renal disease. Accelerated atherosclerosis will then lead to increased prevalence of coronary artery disease, heart failure, stroke, and peripheral arterial disease. Consequently, subjects with chronic renal failure are exposed to increased morbidity and mortality as a result of cardiovascular events. Prevention and treatment of cardiovascular disease are major considerations in the management of individuals with chronic kidney disease.
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PMID:Chronic kidney disease: effects on the cardiovascular system. 1760 56

Metabolic syndrome (MetS) has been defined in different ways. However, key components common to most definitions are a constellation of risk factors including abdominal adiposity, impaired fasting glucose, hypertension, and dyslipidemia. A major mediator of MetS appears to be insulin resistance, which relates to the development of the vascular and metabolic dysfunctions that precede overt cardiovascular disease and type 2 diabetes. Evidence suggests that the mechanisms underlying the elevated cardiovascular risk associated with MetS begin with subclinical organ damage. Therapy for MetS targets individual components of the syndrome and includes lifestyle interventions, lipid-modifying therapy, and antihypertensive agents, particularly those that inhibit the renin-angiotensin system. Results of trials of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers have demonstrated reductions in new-onset diabetes and cardiovascular events in a wide range of patients. Clinical trials to investigate further the role of these drugs in the primary prevention of type 2 diabetes in patients with MetS are currently under way. The purpose of this paper is to review the MetS from the perspective of the cardiology workforce with the hope that a better understanding of the links between MetS and cardiovascular disease could lead to improved management of persons at risk.
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PMID:Metabolic syndrome and cardiovascular disease: challenges and opportunities. 1760 58

Metabolic syndrome is defined as the combination of abdominal obesity, insulin resistance, atherogenic dyslipidemia, and prothrombotic and proinflammatory states. Due to the epidemic proportion of overweight and obesity worldwide and the development of useful clinical tools to identify these patients more easily, metabolic syndrome is increasingly recognized in adults and represents a clear risk factor for the development of both type 2 diabetes and cardiovascular disease. Management of patients with metabolic syndrome is a clinical challenge and requires a multifactorial, multidisciplinary approach. Changes in lifestyle are obviously the first therapeutic step and include both dietary modifications and increased daily exercise. Several questions remain to be elucidated with respect to pharmacological treatment. The blood pressure levels required to initiate antihypertensive treatment, the blood pressure goal to be achieved and the possibility of including a renin-angiotensin system blocker as a part of the pharmacological treatment are still under discussion. The management of atherogenic dyslipidemia is focused on LDL-cholesterol levels, although most patients with metabolic syndrome have normal LDL-cholesterol. There is lack or poor evidence on the need for specific drugs to reduce triglycerides, to increase HDL-cholesterol, to improve insulin sensitivity or to decrease abdominal obesity. There is an urgent need for consensus in the treatment of subjects with metabolic syndrome in order to prevent very high future rates of type 2 diabetes and cardiovascular disease.
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PMID:Management of cardiovascular risk factors in patients with metabolic syndrome. 1763 Sep 47

Arterial hypertension is one of the major coronary risk factors for cardiovascular diseases. In women after menopause blood pressure is increased. The mechanisms responsible for the postmenopausal increase in blood pressure are complex and various factors may have some influence on it. A key-role in etiology of postmenopausal hypertension plays a decrease of estrogen production. Hormone replacement therapy in postmenopausal women does not effect significantly blood pressure values. This suggests that the lower level of estrogens is not only one factor in the etiology of hypertension in women in this period. Various elements have been proposed to play a role in etiology of postmenopausal hypertension, such as activation of the sympathetic nervous system, activation of the renin-angiotensin-aldosterone system, endothelium dysfunction, increase in endothelin and oxidative stress, and more common presence of other risk factors for cardiovascular diseases. These include: dyslipidemia, obesity, glucose intolerance and diabetes mellitus type 2, which are correlated with increased risk of cardiovascular complications of arterial hypertension. It is believed that insulin resistance and hyper-insu-linemia provide a link between these disorders and autonomic dysfunction. Many experimental and clinical studies will be necessary to evaluate the importance of the variety of mechanisms described in this review.
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PMID:[Hypertension in postmenopausal women --selected pathomechanisms]. 1764 47

Chronic kidney disease (CKD) occurs in all age groups, including children. Regardless of the underlying cause, CKD is characterized by progressive scarring that ultimately affects all structures of the kidney. The relentless progression of CKD is postulated to result from a self-perpetuating vicious cycle of fibrosis activated after initial injury. We will review possible mechanisms of progressive renal damage, including systemic and glomerular hypertension, various cytokines and growth factors, with special emphasis on the renin-angiotensin-aldosterone system (RAAS), podocyte loss, dyslipidemia and proteinuria. We will also discuss possible specific mechanisms of tubulointerstitial fibrosis that are not dependent on glomerulosclerosis, and possible underlying predispositions for CKD, such as genetic factors and low nephron number.
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PMID:Mechanisms of progression of chronic kidney disease. 1764 26


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