Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The maintenance of blood vessel homeostasis is closely associated with Reactive Oxygen and Nitrogen Species (ROS and RNS) production in the blood vessel wall. The main molecules taking part in this process are nitric oxide (NO), superoxide anion (O2*-), hydrogen peroxide (H2O2) and their derivatives. The production of these factors occurs in health and disease, however the increased ROS release is often referred to as oxidative stress. While initially oxidative stress was considered systemically, recent data indicate that it occurs locally in subcellular spaces and may be a result of dysfunction of individual enzyme systems. Oxidative stress induces inflammation, proliferation and migration of vascular smooth muscle cells, may regulate apoptosis and the function of the cells of vascular wall, finally leading to dysfunction of endothelium, media and adventitia, leading to cardiovascular diseases such as atherosclerosis, hypertension or heart failure. It is believed that a family of NADPH oxidases is the main source of ROS in the vessel wall, but also in other organs and tissues. It consists of seven known and quite precisely characterized homologues (NOX1, NOX2, NOX3, NOX4, NOX5, DUOX1 and DUOX2) which often have very distinct activity and cellular localization and function. Besides harmful actions, we are beginning to understand the protective effects of ROS and RNS. They have many functions regulating redox-sensitive gene expression and influencing a proper function of cells and vessels. NOX4 has been particularly well characterized in this respect. Thus, the maintenance of the right homeostasis depends not only on ROS removing capabilities, but especially on preserving the adequate level of ROS production.
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PMID:[Oxidative stress and vascular function]. 2474 73

During the development of heart failure in humans and animal models, an increase in reactive oxygen species (ROS) levels was observed. However, there is no information whether this increase of ROS is associated with an increase in the density of specific isoforms of NADPH oxidases (NOXs) 1-5. The objective of this study was to verify whether the densities of NOXs 1-5 change during the development of heart failure. Using the well-known model of cardiomyopathic hamsters, the UM-X 7.1 line, a model that strongly resembles the pathology observed in humans from a morphological and functional point of view, our studies showed that, as in humans, NOXs 1-5 are present in both normal and UM-X7.1 hamster hearts. Even though the densities of NOXs 2 and 5 were unchanged, the levels of both NOXs 1 and 4 significantly decreased in UM-X7.1 hamster hearts during heart failure. These changes were accompanied with a significant increase in NOX3 level. These results suggest that, during heart failure, NOX3 plays a vital role in compensating the decrease of NOXs 1 and 4. This increase in NOX3 may also be responsible, at least in part, for the reported increase in ROS levels in heart failure.
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PMID:Increase of NADPH oxidase 3 in heart failure of hereditary cardiomyopathy 1. 3089 39