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 © 2010 Published by Elsevier Inc. All rights reserved. Trends in Cardiovascular Medicine1050-1738207October 2010 © 2010 Published by Elsevier Inc. All rights reserved. healthpermissions@elsevier.comhttp://www.tcmonline.org/article/PIIS1050173811001095/abstract?rss=yesCover10.1016/S1050-1738(11)00109-5Trends in Cardiovascular Medicine 20, 7 (2010)2010-10-01Trends in Cardiovascular Medicine2010-10-01207S1050-1738(11)X0005-1OFCOFChttp://www.tcmonline.org/article/PIIS1050173811000648/abstract?rss=yes Despite the use of recommended antiplatelet treatment strategies, the presence of diabetes mellitus (DM) has been consistently associated with a higher risk of recurrent ischemic events in patients suffering an acute coronary syndrome. The high prevalence of DM patients presenting with low responsiveness to standard oral antiplatelet treatment regimens contributes to these impaired outcomes. This article provides an overview of the currently available oral antiplatelet agents, focusing on limitations of these therapies in DM patients, and evaluates new antithrombotic treatment strategies that may help overcome these limitations. Oral Antiplatelet Therapy in Patients with Diabetes Mellitus and Acute Coronary SyndromesJosé Luis Ferreiro, Ángel R. Cequier, Dominick J. Angiolillo10.1016/j.tcm.2011.10.001Trends in Cardiovascular Medicine 20, 7 (2010)2010-10-01Trends in Cardiovascular Medicine2010-10-01207S1050-1738(11)X0005-1Review Articles211217http://www.tcmonline.org/article/PIIS1050173811000818/abstract?rss=yes Mutations in the lamin A/C gene (LMNA) encoding A-type nuclear lamins cause dilated cardiomyopathy. We have uncovered a novel connection between these mutations and hyperactivation of the extracellular signal-regulated kinase 1/2 and c-jun N-terminal kinase branches of the mitogen-activated protein kinase signaling pathway in a mouse model of the disease. This discovery has identified targets that can be inhibited by drugs that improve heart function and prevent fibrosis. Mitogen-Activated Protein Kinase Inhibitor Regulation of Heart Function and Fibrosis in Cardiomyopathy Caused by Lamin A/C Gene MutationAntoine Muchir, Wei Wu, Howard J. Worman10.1016/j.tcm.2011.11.002Trends in Cardiovascular Medicine 20, 7 (2010)2010-10-01Trends in Cardiovascular Medicine2010-10-01207S1050-1738(11)X0005-1Review Articles217221http://www.tcmonline.org/article/PIIS1050173811000843/abstract?rss=yes Adrenergic and angiotensin receptors are prominent targets in pharmacological alleviation of cardiac remodeling and heart failure, but their use is associated with cardiodepressant side effects. Recent advances in our understanding of seven transmembrane receptor signaling show that it is possible to design ligands with “functional selectivity,” acting as agonists on certain signaling pathways while antagonizing others. This represents a major pharmaceutical opportunity to separate desired from adverse effects governed by the same receptor. Accordingly, functionally selective ligands are currently pursued as next-generation drugs for superior treatment of heart failure. Therapeutic Potential of Functional Selectivity in the Treatment of Heart FailureGitte Lund Christensen, Mark Aplin, Jakob Lerche Hansen10.1016/j.tcm.2011.11.005Trends in Cardiovascular Medicine 20, 7 (2010)2010-10-01Trends in Cardiovascular Medicine2010-10-01207S1050-1738(11)X0005-1Review Articles221227http://www.tcmonline.org/article/PIIS1050173811000855/abstract?rss=yes Through local cell–cell interactions, the Notch signaling pathway controls tissue formation and homeostasis during embryonic and adult life. In the heart, Notch1 is expressed in a variety of cell types, such as cardiomyocytes, smooth muscle cells, and endothelial cells. In cardiomyocytes, Notch1 is activated in proliferating embryonic and immature cardiomyocytes, and it is downregulated in the myocardium during postnatal development. However, Notch signaling in the adult myocardium could be activated transiently in response to myocardial injury, suggesting that Notch signaling may contribute to cardiac repair. Indeed, activation of Notch1 intracellular domain blunts the severity of myocardial injury and improves myocardial hemodynamic function. Conversely, genetic ablation of the Notch1 gene, either systemically or in bone marrow-derived cells, leads to impaired cardiac repair following myocardial infarction. In this review, we discuss the complex mechanisms of Notch signaling and its role in cardiac repair and regeneration after myocardial infarction. Notch Signaling as an Important Mediator of Cardiac Repair and Regeneration After Myocardial InfarctionYuxin Li, Yukio Hiroi, James K. Liao10.1016/j.tcm.2011.11.006Trends in Cardiovascular Medicine 20, 7 (2010)2010-10-01Trends in Cardiovascular Medicine2010-10-01207S1050-1738(11)X0005-1Review Articles228231http://www.tcmonline.org/article/PIIS1050173811000867/abstract?rss=yes This article provides an overview of the current knowledge on intraplatelet oxidative/nitrative stress, an abnormality associated with platelet activation and hyper-reactivity. The first issue discussed is related to induction of platelet endogenous stress by the molecules present within the circulating (extracellular) milieu that bathes these cells. The second issue concerns the intraplatelet oxidative/nitrative stress associated with specific pathologies or clinical procedures and action of particular molecules and platelet agonists as well as of the specialized intraplatelet milieu and its redox system; the biomarkers of endogenous oxidative/nitrative stress are also briefly outlined. Next, the association between intraplatelet oxidative/nitrative stress and the risk factors of the metabolic syndrome is presented. Then, the most recent strategies aimed at the control/regulation of platelet endogenous oxidative/nitrative stress, such as exploitation of circulating extracellular reactive oxygen species scavengers, manipulation of platelet molecules, and the use of antioxidants, are discussed. Finally, the results of studies on platelet-dependent redox mechanisms, which deserve immediate attention for potential clinical exploitation, are illustrated. Intraplatelet Oxidative/Nitrative Stress: Inductors, Consequences, and ControlNicoleta Alexandru, Doina Popov, Adriana Georgescu10.1016/j.tcm.2011.11.007Trends in Cardiovascular Medicine 20, 7 (2010)2010-10-01Trends in Cardiovascular Medicine2010-10-01207S1050-1738(11)X0005-1Review Articles232238http://www.tcmonline.org/article/PIIS1050173811000892/abstract?rss=yes Congenital heart diseases associated with increased pulmonary blood flow commonly leads to the development of pulmonary hypertension. However, most patients who undergo histological evaluation have advanced pulmonary hypertension, and therefore it has been difficult to investigate aberrations in signaling cascades that precede the development of overt vascular remodeling. This review discusses the role played by both oxidative and nitrosative stress in the lung and their impact on the signaling pathways that regulate vasodilation, vessel growth, and vascular remodeling in the neonatal lung exposed to increased pulmonary blood flow. Oxidative Stress and the Development of Endothelial Dysfunction in Congenital Heart Disease With Increased Pulmonary Blood Flow: Lessons From the Neonatal LambSaurabh Aggarwal, Christine Gross, Jeffrey R. Fineman, Stephen M. Black10.1016/j.tcm.2011.11.010Trends in Cardiovascular Medicine 20, 7 (2010)2010-10-01Trends in Cardiovascular Medicine2010-10-01207S1050-1738(11)X0005-1Review Articles238246http://www.tcmonline.org/article/PIIS1050173812000047/abstract?rss=yesReferring to: LeClair R, Lindner V: 2007. The role of collagen triple helix repeat containing 1 in injured arteries, collagen expression, and transforming growth factor β signaling. Trends in Cardiovascular Medicine 17:202-205.Erratum10.1016/j.tcm.2012.01.003Trends in Cardiovascular Medicine 20, 7 (2010)2010-10-01Trends in Cardiovascular Medicine2010-10-01207S1050-1738(11)X0005-1Erratum247247http://www.tcmonline.org/article/PIIS1050173811001113/abstract?rss=yesContents10.1016/S1050-1738(11)00111-3Trends in Cardiovascular Medicine 20, 7 (2010)2010-10-01Trends in Cardiovascular Medicine2010-10-01207S1050-1738(11)X0005-1FrontmatterA1A1http://www.tcmonline.org/article/PIIS1050173811001125/abstract?rss=yesTCM Editorial Policy10.1016/S1050-1738(11)00112-5Trends in Cardiovascular Medicine 20, 7 (2010)2010-10-01Trends in Cardiovascular Medicine2010-10-01207S1050-1738(11)X0005-1FrontmatterA2A2