Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:Q8IXL6 (RNS)
 1,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chemical as well as cytophotometric studies were carried out on myocardium of cardiomyopathic hamsters of strain BIO 8262 and of healthy control hamsters of strain CLAC. Our interest was to find out whether the cardiomyopathic hamsters suffer from hypertrophic cardiomyopathy or not. The heart muscle mass was only slightly increased in the older cardiomyopathic hamsters when compared with the controls. This increase was accompanied by an elevated content of total DNS, RNS and protein. Furthermore, the number of hyperdiploid heart muscle cells was slightly increased in the older diseased animals. However, all these changes were of minor degree. Thus, a distinct hypertrophying process in the myocardium of the cardiomyopathic hamsters can be excluded. On the other hand, the connective tissue components (polysaccharides and collagen) were distinctly increased in the hearts of older cardiomyopathic hamsters. This is in accordance with morphological investigations, in which replacement of necrotic myocardium by fibrosis could be detected.
Basic Res Cardiol
PMID:The cardiomyopathy of the Syrian hamster (strain BIO 8262)--hypertrophic or dystrophic? 14 86

Although the mitochondrial permeability transition pore (mPTP) was first discovered almost 30 years ago [1], it did not attract significant research attention until the 1990's when several studies implicated mPTP in apoptosis [2]. Today, the dogma suggests that opening of mPTP is detrimental to the cell and mPTP activation is widely thought to contribute to disease in cancer, neurodegenerative diseases, stroke, muscular dystrophy, and cardiac reperfusion injury [3]. Multiple factors including Ca(2+), OH(-), P(i), cyclophilin D, reactive oxygen and nitrogen species (ROS and RNS) trigger mPTP opening [4]. However, whether mPTP activation feeds back to alter mitochondrial ROS generation remains unclear. We recently demonstrated that under normal conditions, individual mitochondria undergo spontaneous transient bursts of quantal superoxide generation, termed "superoxide flashes" [5]. Superoxide flashes are observed in all cell types investigated to date and are triggered by a surprising functional coupling between mPTP activation and electron transport chain (ETC) dependent superoxide production. Additionally, reoxgenation following anoxia leads to uncontrolled superoxide flash genesis in cardiomyocytes. This positive feedback mechanism for mPTP/ETC-dependent ROS generation may drive localized redox signaling in individual mitochondria under physiological conditions, and when left unchecked, contribute to global cellular oxidative stress under pathological conditions in cardiac disease. The mPTP activity-dependent cell life and death determination imposes new challenges and opportunities in the pursuit of therapeutic agents for treating diseases in which oxidative stress has been implicated such as cardiac ischemia-reperfusion injury.
Future Cardiol 2008 Nov 01
PMID:Superoxide flashes: illuminating new insights into cardiac ischemia/reperfusion injury. 1964 73

Coronary artery disease is a major cause of morbidity and mortality in the Western countries. Acute myocardial infarction is a serious and often lethal consequence of coronary artery disease, resulting in contractile dysfunction and cell death. It is well known that unbalanced and high steady state levels of reactive oxygen and nitrogen species (ROS/RNS) are responsible for cytotoxicity, which in heart leads to contractile dysfunction and cell death. Pre- and post-conditioning of the myocardium are two treatment strategies that reduce contractile dysfunction and the amount of cell death considerably. Paradoxically, ROS and RNS have been identified as a part of cardioprotective signaling molecules, which are essential in pre- and post-conditioning processes. S-nitrosylation of proteins is a specific posttranslational modification that plays an important role in cardioprotection, especially within mitochondria. In fact, mitochondria are of paramount importance in either promoting or limiting ROS/RNS generation and reperfusion injury, and in triggering kinase activation by ROS/RNS signaling in cardioprotection. These organelles are also the targets of acidosis, which prevents mitochondrial transition pore opening, thus avoiding ROS-induced ROS release. Therefore, we will consider mitochondria as either targets of damage or protection from it. The origin of ROS/RNS and the cardioprotective signaling pathways involved in ROS/RNS-based pre- and post-conditioning will be explored in this article. A particular emphasis will be given to new aspects concerning the processes of S-nitrosylation in the cardioprotective scenario.
Basic Res Cardiol 2013 Nov
PMID:Redox balance and cardioprotection. 2415 92