Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peripheral Artery Disease (PAD) is a strong predictor of MI, stroke and death due to vascular causes. PAD affects 8-12 million people in the United States. As the population lives longer with chronic diseases, researchers estimate that the incidence of PAD will increase, likely increasing myocardial infarction, stroke and death. This paper reviews the epidemiology, pathophysiology, risk factors, treatment and management of PAD. With improved understanding of the disease process, risk factors and treatment, clinicians will be able to detect PAD earlier, provide diagnosis, treat and manage this disease. PAD is associated with reduced quality of life, and persons with PAD are also at risk of developing coronary artery disease and cerebrovascular disease. Better clinical evaluation and routine screening are important in identifying and treating patients at risk for PAD. All patients with PAD should receive risk-factor modification, such as treatment and education, about smoking cessation, blood pressure control and lowering of cholesterol. Appropriate pharmacological management includes antiplatelet therapy of aspirin, use of clopidogrel for those individuals who are sensitive to aspirin. Patients who have had bypass surgery or stent placement require dual antiplatelet therapy of aspirin and clopidogrel. The American Heart Association (AHA) states that treatment with beta-blockers and ACE inhibitors is appropriate pharmacotherapy to treat PAD. Other FDA approved medications such as Cilostazol and Pentoxifylline are also used in the treatment of pain associated with intermittent claudication.
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PMID:Peripheral arterial disease: Pathophysiology, risk factors, diagnosis, treatment, and prevention. 1948 52

Cilostazol (CILO), a selective inhibitor of phosphodiesterase 3 with potent antithrombotic property, has been shown to have a vasculoprotective effect in atherosclerosis animal models due to its potential anti-inflammatory and antioxidant actions. This study was undertaken to investigate whether CILO has in fact any vasculoprotective effects in aldosterone-induced hypertensive rats (Aldo-rats), and whether CILO affects Aldo-induced oxidative stress, nitric oxide (NO) production and pro-inflammatory gene expression. Treatment with CILO markedly ameliorated perivascular inflammatory changes in the coronary arterioles of Aldo-rats without affecting the systolic blood pressure and left ventricular weight. Treatment with CILO also prevented the increase in plasma levels of thiobarbituric acid-reactive substances, an oxidative stress marker, as well as decreased urinary NOx excretion in Aldo-rats. Furthermore, CILO almost completely inhibited a set of upregulated proinflammatory genes (ICAM-1, MCP-1, PDGF-A, osteopontin, MMP-2 and ACE), as well as NAD(P)H oxidase components (p22phox, gp91phox, p47phox) and Aldo-inducible genes (SGK-1 and NHE-1) in the aortic tissues from Aldo-rats. Taken together, this study showed for the first time that CILO prevented Aldo-induced vascular inflammation and injury without affecting the blood pressure, suggesting its vasculoprotective effect on Aldo-induced vascular injury independent of blood pressure.
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PMID:Vasculoprotective effect of cilostazol in aldosterone-induced hypertensive rats. 2001 1