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 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 Medicine1050-1738196August 2009 © 2010 Published by Elsevier Inc. All rights reserved. healthpermissions@elsevier.comhttp://www.tcmonline.org/article/PIIS1050173810000095/abstract?rss=yesCover 110.1016/S1050-1738(10)00009-5Trends in Cardiovascular Medicine 19, 6 (2009)2009-08-01Trends in Cardiovascular Medicine2009-08-01196S1050-1738(10)X0002-0OFCOFChttp://www.tcmonline.org/article/PIIS1050173809001674/abstract?rss=yesSeryl-transfer RNA synthetase (Sars) is one of the 20 aminoacyl-transfer RNA synthetases that are enzymes essential for protein synthesis; however, the developmental function of Sars has not been elucidated. In zebrafish, impairment of zygotic Sars function leads to a significant dilatation of the aortic arch vessels and aberrant branching of cranial and intersegmental vessels. This abnormal vascular branching in sars mutants can be suppressed by a form of Sars that lacks canonical function, indicating that a noncanonical activity of Sars regulates vascular development. Inhibition or knockdown of vascular endothelial growth factor (Vegf) signaling, which plays pivotal roles in the establishment of the vascular network, suppresses the abnormal vascular branching observed in sars mutants. Here, we discuss the possible functional relationship between Sars function and Vegf signaling.Noncanonical Activity of Seryl-Transfer RNA Synthetase and Vascular DevelopmentAtsuo Kawahara, Didier Y.R. Stainier10.1016/j.tcm.2009.11.001Trends in Cardiovascular Medicine 19, 6 (2009)2009-08-01Trends in Cardiovascular Medicine2009-08-01196S1050-1738(10)X0002-0Review Articles179182http://www.tcmonline.org/article/PIIS1050173809001790/abstract?rss=yesIntercalated disks (ICDs) are highly organized cell-cell adhesion structures, which connect cardiomyocytes to one another. They are composed of three major complexes: desmosomes, fascia adherens, and gap junctions. Desmosomes and fascia adherens junction are necessary for mechanically coupling and reinforcing cardiomyocytes, whereas gap junctions are essential for rapid electrical transmission between cells. Because human genetics and mouse models have revealed that mutations and/or deficiencies in various ICD components can lead to cardiomyopathies and arrhythmias, considerable attention has focused on the biologic function of the ICD. This review will discuss recent scientific developments related to the ICD and focus on its role in regulating cardiac muscle structure, signaling, and disease.Cell-Cell Connection to Cardiac DiseaseFarah Sheikh, Robert S. Ross, Ju Chen10.1016/j.tcm.2009.12.001Trends in Cardiovascular Medicine 19, 6 (2009)2009-08-01Trends in Cardiovascular Medicine2009-08-01196S1050-1738(10)X0002-0Review Articles182190http://www.tcmonline.org/article/PIIS1050173809001807/abstract?rss=yesEndothelial dysfunction/death is an initial event for the development of atherosclerosis occurring in the areas of arteries where blood flow is disturbed. Recent data indicated that rapid turnover of endothelial cells in atherosclerosis-prone areas is followed by endothelial repair. The mechanisms of endothelial death/proliferation in these areas related to altered blood flow involve different signal pathways, for example, endoplasmic reticulum stress-X-box binding protein 1-caspase for apoptosis and vascular endothelial growth factor receptor-histone deacetylase 3-Akt for the survival. The present review aims to update the progress in endothelial turnover in response to disturbed flow and to discuss the underlining mechanisms in the development of atherosclerosis.Disturbed Flow-Enhanced Endothelial Turnover in AtherosclerosisQingbo Xu10.1016/j.tcm.2009.12.002Trends in Cardiovascular Medicine 19, 6 (2009)2009-08-01Trends in Cardiovascular Medicine2009-08-01196S1050-1738(10)X0002-0Review Articles191195http://www.tcmonline.org/article/PIIS1050173809001819/abstract?rss=yesSeveral high-profile failures of lipid-related therapeutics in clinical trials have led to intense interest in improved discovery and preclinical prioritization of potential targets. The careful study of patients with rare monogenic disorders has played a key role in establishing the causal role of cholesterol in atherosclerosis and highlighting viable drug targets. Systematic efforts to extend the association of common variants linked with lipid levels to coronary disease enable assessment of the vascular consequences of lifelong differences in lipids due to variation in specific molecules. This application of genetic epidemiology, termed Mendelian randomization, may prove useful in informing ongoing drug development efforts.Discovery and Validation of New Molecular Targets in Treating Dyslipidemia: The Role of Human GeneticsAmit V. Khera, Daniel J. Rader10.1016/j.tcm.2009.12.003Trends in Cardiovascular Medicine 19, 6 (2009)2009-08-01Trends in Cardiovascular Medicine2009-08-01196S1050-1738(10)X0002-0Review Articles195201http://www.tcmonline.org/article/PIIS1050173809001832/abstract?rss=yesThere has been growing interest in targeting myocardial substrate metabolism for the therapy of cardiovascular and metabolic diseases. This is largely based on the observation that cardiac metabolism undergoes significant changes during both physiologic and pathologic stresses. In search for an effective therapeutic strategy, recent studies have focused on the functional significance of the substrate switch in the heart during stress conditions, such as cardiac hypertrophy and failure, using both pharmacologic and genetic approaches. The results of these studies indicate that both the capacity and the flexibility of the cardiac metabolic network are essential for normal function; thus, their maintenance should be the primary goal for future metabolic therapy.Metabolic Therapy at the Crossroad: How to Optimize Myocardial Substrate Utilization?Stephen C. Kolwicz, Rong Tian10.1016/j.tcm.2009.12.005Trends in Cardiovascular Medicine 19, 6 (2009)2009-08-01Trends in Cardiovascular Medicine2009-08-01196S1050-1738(10)X0002-0Review Articles201207http://www.tcmonline.org/article/PIIS1050173809001844/abstract?rss=yesAbstract: In traditional pure protein high-throughput drug screens, also called in vitro screens, individual compounds from a small molecule collection are tested to determine whether they inhibit the enzymatic activity or binding properties of a purified target protein. In contrast, phenotypic high-throughput drug screens, also called chemical genetic or in vivo screens, investigate the ability of individual compounds from a collection to inhibit a biological process or disease model in live cells or intact organisms. In this review, the role of phenotypic screening techniques to identify novel therapeutic agents for the treatment of cardiovascular disease will be discussed.The Application of Phenotypic High-Throughput Screening Techniques to Cardiovascular ResearchYoram Etzion, Anthony J. Muslin10.1016/j.tcm.2009.12.006Trends in Cardiovascular Medicine 19, 6 (2009)2009-08-01Trends in Cardiovascular Medicine2009-08-01196S1050-1738(10)X0002-0Review Articles207212http://www.tcmonline.org/article/PIIS1050173810000113/abstract?rss=yesContents10.1016/S1050-1738(10)00011-3Trends in Cardiovascular Medicine 19, 6 (2009)2009-08-01Trends in Cardiovascular Medicine2009-08-01196S1050-1738(10)X0002-0FrontmatterA1A1http://www.tcmonline.org/article/PIIS1050173810000125/abstract?rss=yesTCM Editorial Policy10.1016/S1050-1738(10)00012-5Trends in Cardiovascular Medicine 19, 6 (2009)2009-08-01Trends in Cardiovascular Medicine2009-08-01196S1050-1738(10)X0002-0FrontmatterA2A2