Trends in Cardiovascular Medicine RSS feed: Current Issue. Trends in Cardiovascular Medicine provides state-of-the-art reviews on the application of scientific advances to the development of new prognostic, diagnostic, and therapeutic strategies for heart and vascular diseases. The areas covered include basic and clinical research, including genetic studies of human cardiovascular diseases, therapeutic angiogenesis, cardiovascular gene therapy, cardiac development and congenital heart disease, channel regulation and arrhythmogenesis, coagulation disorders, novel therapeutic targets and agents, thrombotic disorders, molecular advances in hypertrophy and heart failure, genetically engineered animal models of human disease, and new insights into atherosclerotic heart disease. http://www.tcmonline.org/?rss=yesElsevier Inc.en © 2011 Published by Elsevier Inc. All rights reserved. Trends in Cardiovascular Medicine1050-1738212February 2011 © 2011 Published by Elsevier Inc. All rights reserved. healthpermissions@elsevier.comhttp://www.tcmonline.org/article/PIIS1050173812000655/abstract?rss=yesCover10.1016/S1050-1738(12)00065-5Trends in Cardiovascular Medicine 21, 2 (2011)2011-02-01Trends in Cardiovascular Medicine2011-02-01212S1050-1738(12)X0004-5OFCOFChttp://www.tcmonline.org/article/PIIS1050173812000266/abstract?rss=yes Inflammation plays a crucial role in the pathophysiology of myocardial infarction (MI). In particular, reperfusion caused by increased thrombolytic activity or revascularization therapy may restore the coronary blood flow and reduce the infarct size, but it also simultaneously enhances the inflammatory response and causes harmful effects on the myocardium—a process termed ischemia-reperfusion (I/R) injury. The inflammasome is a large multiprotein complex that is formed in the cytosol in response to danger signals; it drives the proinflammatory cytokine interleukin (IL)-1β. Increasing evidence indicates that the inflammasome is a key player in the disease processes of sterile inflammation. In particular, IL-1β is a prominent and early mediator of inflammation in I/R injury, suggesting the importance of the inflammasome in myocardial I/R injury. This article reviews the role of the inflammasome in the development of myocardial I/R injury and discusses the potential of the inflammasome as a novel therapeutic target for the treatment of myocardial I/R injury. Role of the Inflammasome in Myocardial InfarctionMasafumi Takahashi10.1016/j.tcm.2012.02.002Trends in Cardiovascular Medicine 21, 2 (2011)2011-02-01Trends in Cardiovascular Medicine2011-02-01212S1050-1738(12)X0004-5Review Articles3741http://www.tcmonline.org/article/PIIS1050173812000278/abstract?rss=yes Clinical trials have clearly demonstrated that mineralocorticoid receptor (MR) blockade improves outcome in patients with chronic systolic heart failure and left ventricular dysfunction after myocardial infarction; however, the underlying mechanisms as well as the cell-specific functional role of MR activation are still under investigation. Extrarenal effects of MR blockade on cardiovascular extracellular matrix turnover and oxidative stress, on myocardial structural and electrical remodeling, and on sympathoadrenergic stimulation, platelet activation, endothelial dysfunction, and macrophage polarization appear to be important mechanisms. Recent scientific advances, involving mice with cardiomyocyte-restricted inactivation of the MR gene suggest that the clinical benefits of MR blocking therapy in myocardial infarction and heart failure are mediated largely via cardiomyocyte-dependent mechanisms, and they provide strong evidence that more favorable effects on cardiac dysfunction and failure can be achieved by early initiation of MR blockade postinfarction. Cardiomyocyte Mineralocorticoid Receptor Function Post Myocardial InfarctionDaniela Fraccarollo, Johann Bauersachs10.1016/j.tcm.2012.02.003Trends in Cardiovascular Medicine 21, 2 (2011)2011-02-01Trends in Cardiovascular Medicine2011-02-01212S1050-1738(12)X0004-5Review Articles4247http://www.tcmonline.org/article/PIIS105017381200028X/abstract?rss=yes Ryanodine receptor (RyR2) dysfunction, which may result from a variety of mechanisms, has been implicated in the pathogenesis of cardiac arrhythmias and heart failure. In this review, we discuss the important role of Ca2+/calmodulin-dependent protein kinase II (CaMKII) in the regulation of RyR2-mediated Ca2+ release. In particular, we examine how pathological activation of CaMKII can lead to an increased risk of sudden arrhythmic death. Finally, we discuss how reduction of CaMKII-mediated RyR2 hyperactivity might reduce the risk of arrhythmias and may serve as a rationale for future pharmacotherapeutic approaches. Ryanodine Receptor Phosphorylation, Calcium/Calmodulin-Dependent Protein Kinase II, and Life-Threatening Ventricular ArrhythmiasMark D. McCauley, Xander H.T. Wehrens10.1016/j.tcm.2012.02.004Trends in Cardiovascular Medicine 21, 2 (2011)2011-02-01Trends in Cardiovascular Medicine2011-02-01212S1050-1738(12)X0004-5Review Articles4851http://www.tcmonline.org/article/PIIS1050173812000369/abstract?rss=yes Traditionally, the adult heart has been viewed as a terminally differentiated postmitotic organ in which the number of cardiomyocytes is established at birth and these cells persist throughout the life span of the organ and organism. However, the discovery that cardiac stem cells live in the heart and differentiate into the various cardiac cell lineages has dramatically changed our understanding of myocardial biology. Deciphering the biological processes that lead to myocyte renewal is a challenging task. Cardiac regeneration may be accomplished by (1) commitment of multipotent stem cells that generate all specialized lineages within the parenchyma, (2) activation of unipotent progenitors with restricted differentiation potential, (3) replication of pre-existing differentiated cells, (4) transdifferentiation of exogenous progenitors that undergo plastic conversion into cells different from the organ of origin, and (5) dedifferentiation of cardiomyocytes that re-enter the cell cycle and divide. These multiple mechanisms of cell growth may act in concert to regenerate complex structures and restore the function of the target organ. Mechanisms of Myocardial RegenerationAnnarosa Leri, Jan Kajstura, Piero Anversa10.1016/j.tcm.2012.02.006Trends in Cardiovascular Medicine 21, 2 (2011)2011-02-01Trends in Cardiovascular Medicine2011-02-01212S1050-1738(12)X0004-5Review Articles5258http://www.tcmonline.org/article/PIIS1050173812000382/abstract?rss=yes Recent studies have consistently demonstrated that neuronal nitric oxide synthase (nNOS) is cardioprotective in different disease states. nNOS has been shown to delay transition to heart failure in response to pressure overload, to protect the myocardium from functional deterioration after myocardial infarction, and to decrease mortality after myocardial infarction. Recent work identified the precise molecular mechanisms of nNOS action in the myocardium during rest and after myocardial damage. In animal models with nNOS overexpression restricted to cardiac myocytes and nNOS−/− mice, it was consistently demonstrated that nNOS decreased myocardial contractility via inhibition of the ICa,L amplitude and [Ca2+]i transients. The mitochondria and xanthine oxidoreductase were identified as further targets for nNOS in cardiac disease models. In this review, we focus on the protective effects of nNOS after ischemia-reperfusion injury, with emphasis on the subcellular localization of nNOS and its putative targets. Role of nNOS in Cardiac Ischemia-Reperfusion InjuryJörn Strasen, Oliver Ritter10.1016/j.tcm.2012.03.001Trends in Cardiovascular Medicine 21, 2 (2011)2011-02-01Trends in Cardiovascular Medicine2011-02-01212S1050-1738(12)X0004-5Review Articles5863http://www.tcmonline.org/article/PIIS1050173812000679/abstract?rss=yesContents10.1016/S1050-1738(12)00067-9Trends in Cardiovascular Medicine 21, 2 (2011)2011-02-01Trends in Cardiovascular Medicine2011-02-01212S1050-1738(12)X0004-5FrontmatterA1A1http://www.tcmonline.org/article/PIIS1050173812000680/abstract?rss=yesTCM Editorial Policy10.1016/S1050-1738(12)00068-0Trends in Cardiovascular Medicine 21, 2 (2011)2011-02-01Trends in Cardiovascular Medicine2011-02-01212S1050-1738(12)X0004-5FrontmatterA2A2