Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Valve replacement is the only long-term effective treatment for calcific aortic valve stenosis. However, this treatment is aimed only at patients with advanced leaflet disease and symptoms of left ventricular obstruction. Over the past 15 years, our understanding of the pathogenesis of calcific aortic stenosis has changed significantly: away from a passive degenerative disease to an active process involving endothelial dysfunction, lipid accumulation, an inflammatory infiltrate, and a regulated process of calcification. Since many of the same processes are characteristic of atherosclerosis, trials have been undertaken to test whether medical therapy (statins, renin-angiotensin inhibition) can prevent or alter the disease course. Although retrospective and non-randomized studies suggested a positive effect with statins, benefit has not been seen in perspective randomized controlled trials, although two major studies are still in progress. Inhibition of renin-angiotensin has shown discordant results in retrospective studies with no randomized controlled data published. In the future, we need to consider other medical therapies that might target different pathways in this disease process. In addition, we need to define the optimal timing and duration of therapy for this chronic slowly progressive disease; treatments aimed at the early disease process may be ineffective with end-stage tissue changes.
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PMID:Prevention of calcific aortic valve stenosis-fact or fiction? 1872 96

Thoracic aortic aneurysms (TAA) often represent the final manifestation of hereditary or degenerative disease processes. TAA are primarily caused by age-related degenerative changes. In this article, the authors highlight the most common pathophysiologic mechanisms responsible for TAA formation and review the paucity of evidence supporting the spectrum of medical therapies for TAA other than renin-angiotensin inhibition. More clinical trials on TAA are required before medical therapies such as beta-blockers, statins, and macrolide antibiotics can be recommended.
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PMID:Does medical therapy for thoracic aortic aneurysms really work? Are beta-blockers truly indicated? CON. 2045 40

Mitral valve prolapse (MVP) represents a common degenerative disease, often requiring surgery. If untreated, MVP with considerable valve incompetence can lead to cardiovascular and systemic complications causing substantial morbidity and mortality. In contrast with the wide knowledge concerning clinical and physiological features, currently available data regarding its molecular bases are very limited. We review current knowledge concerning MVP biological mechanisms, focusing on specific aspects of haemostasis, platelet function, oxidative stress, extracellular matrix remodeling and genomics. In particular, available evidence supports the role played by tissue remodeling processes in determining MVP onset and progression. Moreover, even if a consistent although controversial perturbation of haemostatic system and alterations of the oxidative stress equilibrium have been proposed to influence disease development, it is unknown whether these changes precede or follow MVP occurrence. Consequently, the complete knowledge of all the biochemical pathways involved are far from complete. In addition, changes in the regulation pattern of adrenergic and renin-angiotensin-aldosterone systems have been described in MVP syndrome, a condition characterized by the association of MVP with other peculiar neurological and general symptoms, but it is unknown whether these abnormalities are shared by "traditional" MVP. In conclusion, MVP is probably a multi-factorial process, and many aspects still need to be clarified. As surgery can only correct the damaged valve but not the underlying mechanisms, a more complete knowledge of the involved molecular pathways is necessary, as it may allow the discovery of targeted therapeutic strategies aimed at modifying or slackening MVP natural course in the early phases.
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PMID:Biology of mitral valve prolapse: the harvest is big, but the workers are few. 2116 28

Alzheimer's disease (AD) is an incurable degenerative disease of the central nervous system, leading to dementia. The basis of AD is neurodegenerative process that leads to death of neurons in the cerebral cortex. This neurodegenerative process is associated with the formation of neurofibrillary tangles in the brain and the deposition of senile plaques, the main component of which is a beta-amyloid peptide (Abeta). Risk factors for AD are age, as well as hypertension, atherosclerosis, diabetes and hypercholesterolemia in the pathogenesis of which involved angiotensin converting enzyme (ACE)--key enzyme of the renin-angiotensin (RAS) and kallikrein-kinin (KKS) systems. Recently it was discovered that ACE, along with other metallopeptidases, participates in the metabolism of Abeta, cleaving the bonds at the N-terminal and C-terminal region of the molecule Abeta. The role of the ACE in the degradation processes of Abeta takes an interest. It is associated with the fact that the using of ACE inhibitors is the main therapeutic approach used in the treatment of various forms of hypertension and other cardiovascular diseases. However, until now not been resolved, can be used antihypertensive drugs that inhibit RAS for the treatment or prevention of AD. Currently, there are numerous studies on finding the relationship between RAS and AD.
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PMID:[Angiotensin converting enzyme and Alzheimer's disease]. 2365 Jul 20