Vascular Biology

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Louis J Ignarro - One of the best experts on this subject based on the ideXlab platform.

Joseph Loscalzo - One of the best experts on this subject based on the ideXlab platform.

  • The evolution of the discipline of Vascular Biology: from systems physiology to molecular Biology to molecular systems.
    Circulation research, 2003
    Co-Authors: Joseph Loscalzo
    Abstract:

    The changes in Vascular research over the past half century have been nothing short of extraordinary. From the evolution in technologies to the analytical process, advances that were not even imaginable 50 years ago have led to far-reaching insights into the Biology of the blood vessel and the diseases that affect it. This period has also witnessed two major shifts in the general experimental paradigm of Vascular Biology. At mid-century, Vascular biologists used physiological methods to attempt to understand phenotype. Their primary focus was on Vascular tone and its neurohumoral determinants in health and disease. Limited by available methods, they were essentially unable to apply biochemical or molecular analysis to the characterization of Vascular function. That situation, however, changed approximately 25 years later by which time modern techniques of cell culture were applied to Vascular cells, and microanalytical methods, as well as novel reagents, became available for more precise molecular characterization of Vascular phenotype. Of note, both of these historical phases of research in Vascular Biology used the conventional analytical regimen of reductionism: an investigator typically identified a Vascular reflex or endothelial product of primary interest, asked a scientific question about the role of this reflex or molecule on Vascular phenotype, designed experiments and controls that focused on that question, then drew inferences from the observed experimental result—without regard for other factors in the vessel that might influence the observed phenomenon. In the past decade, another major shift in the investigative paradigm has been developing as a result of access to large molecular data sets. The human genome project, together with expression array analysis, proteomics, and metabolomics, has begun to yield a rich treasure trove of data that offers the promise of great insight into understanding Vascular Biology and pathoBiology. Yet, we are plagued by the limitations of conventional reductionist …

  • Nitric oxide in Vascular Biology
    Journal of thrombosis and haemostasis : JTH, 2003
    Co-Authors: G. Walford, Joseph Loscalzo
    Abstract:

    Summary.  Nitric oxide is a highly versatile heterodiatomic molecule that effects a variety of actions in the vasculture. Originally identified as a principal determination of Vascular tone, nitric oxide has since been recognized to exert anti thrombotic, antiproliferative, and anti-inflammatory effects in the vasculture. At higher concentrations and in the setting of other oxidants, nitric oxide can promote Vascular pathology. In this review, we summarize the molecular mechanisms of nitric oxides actions in Vascular Biology and pathology.

  • Clinical importance of understanding Vascular Biology.
    Experimental nephrology, 2000
    Co-Authors: Jane A Leopold, Joseph Loscalzo
    Abstract:

    A comprehensive understanding of the Biology of the vessel wall has fostered the discovery of novel therapeutic interventions. The Vascular endothelium, smooth muscle cells, and adventitial fibroblasts exist in a tightly regulated milieu in which extraVascular stimuli produce coordinated physiologic actions in each cell type, which, in turn, modulate integrative responses in the vessel wall. When Vascular injury occurs as a result of biochemical or mechanical forces, such as in hypertension, atherosclerosis, or restenosis, normal homeostatic mechanisms are perturbed, and if compensatory mechanisms are overwhelmed, the vessel becomes dysfunctional. These states are characterized by changes in regulatory molecules that stimulate aberrant responses. Recent advances in molecular Biology, including gene transfer and antisense technology, have been used successfully to replete or diminish these factors and restore Vascular homeostasis. We present an overview of basic Vascular Biology as it relates to relevant clinical Vascular pathoBiology and molecular therapeutics.

Donald D. Heistad - One of the best experts on this subject based on the ideXlab platform.

  • Arteriosclerosis, Thrombosis, and Vascular Biology , 1999–2007
    Arteriosclerosis Thrombosis and Vascular Biology, 2007
    Co-Authors: Donald D. Heistad
    Abstract:

    This year marks the end of the Iowa City/Fukuoka/Stockholm editorship for Arteriosclerosis, Thrombosis, and Vascular Biology . As we look forward to the transition to new editors in a few months, we will look back on the growth of the journal. Since the first issue in 1981, Arteriosclerosis, Thrombosis, and Vascular Biology has grown in length of title (from Arteriosclerosis ), frequency (from bi-monthly), number of manuscripts received (now third among the five AHA journals), and impact factor (also third among AHA journals). The major goal of our editorship has been to publish high-quality papers that scientists are eager to read. We built on the foundation laid by previous editors, Edwin Bierman (1981–1991) and Alan Fogelman (1991–1999). The journal arguably was and is the premier journal in studies of lipoproteins and mechanisms of atherosclerosis. We perceived that there was an opportunity to become the premier journal in Vascular Biology. In relation to thrombosis, we focused on developing ATVB as a leading journal for studies of the interaction of blood components with the blood vessel wall. We will summarize some ways that we sought to achieve our goals, and objective parameters which suggest progress toward the goals. There is a great opportunity for Mark Taubman, the new editor, (and the scientific community that benefits from a strong journal) to facilitate the continued growth of the journal. Our intangible goals were to publish a journal that scientists look forward to reading and to which they are eager to submit their manuscripts. Intangible goals are personal, not universal, and therefore challenging to achieve. Some of our more specific goals were: To become the leading journal in Vascular Biology To emphasize timely topics. We have tried to identify and highlight “hot” areas of research with Editorials and Brief Reviews. Readability of the Journal. We have …

  • Arteriosclerosis, Thrombosis, and Vascular Biology, 2006
    Arteriosclerosis Thrombosis and Vascular Biology, 2006
    Co-Authors: Donald D. Heistad
    Abstract:

    We will again provide for our readers an update of the state of the journal. The original goals of our editorship, which began in 1999, were to publish high-quality papers, provide authors with timely review and publication of their manuscripts, and publish papers of interest to our readers. We will summarize data related to each of these goals, some changes and plans for the journal, and thank several groups of people for their help. It is clear that there is no perfect way to evaluate quality of papers published in journals. Nevertheless, impact factor is one measure of quality of papers. Decisions about promotion and tenure are sometimes based in part on impact factor of journals in which papers are published. Thus, impact factor may be important to authors, in relation to selection of journals in which they wish to publish their work. The impact factor for ATVB again increased this past year, from 6.8 to 7.4 (Figure 1). The impact factor of the journal has increased more than 90% during the past few years. Impact factors of other journals in this area of research have not changed consistently during the last few years (Figure 1). We believe that ATVB is generally recognized as an appropriate forum for publication of excellent papers related to atherosclerosis, lipoproteins, Vascular Biology, and thrombosis. Figure 1. Impact factor of ATVB . Immediacy index provides information about the frequency of references to articles during the first year of their publication. The immediacy index for ATVB has increased substantially in the past few years (Figure 2) and may be a predictor of future increases in impact factor. Figure 2. Immediacy Index of ATVB . We try to provide expert and …

  • Arteriosclerosis, Thrombosis, and Vascular Biology, 2005
    Arteriosclerosis Thrombosis and Vascular Biology, 2005
    Co-Authors: Donald D. Heistad
    Abstract:

    The purpose of this editorial is to provide for our readers the annual update of the status of the journal. Goals of our editorship, which began in 1999, were to publish high-quality papers, provide authors with timely review and publication of their manuscripts, and to publish papers of interest to our readers. We will summarize data related to each of these goals, some changes and plans for the journal, and thank several people for their help. There is no perfect approach to evaluate journals and the quality of papers published in journals. Impact factor is one measure of quality of papers. In some Universities, decisions about promotion and tenure are based in part on impact factor of journals in which papers are published. Thus, impact factor may be important, in relation to selection of journals in which authors wish to publish their work. The impact factor for ATVB again increased this past year, to 6.8 (Figure 1). The impact factor of the journal has increased more than 70% during the past few years. The large increase in 1999 was determined by decisions during the editorship of Dr Alan Fogelman. Impact factors of other journals in this area of research have not changed consistently during the last few years (Figure 1). We believe that Arteriosclerosis, Thrombosis, and Vascular Biology is recognized as an appropriate forum for publication of excellent papers related to atherosclerosis, lipoproteins, Vascular Biology, and thrombosis. Figure 1. Impact factor of ATVB , JBC ( Journal of Biological Chemistry ), T&H ( Thrombosis & Hemostatsis ), JLR ( Journal of Lipid Research ), Athero ( Atherosclerosis ) and AJP ( American Journal of Physiology – Heart and Circulation ) Immediacy index provides information about the frequency of references to articles during the first year of their publication. The immediacy index for ATVB has increased substantially in the past …

  • Arteriosclerosis, Thrombosis, and Vascular Biology , 2003
    Arteriosclerosis Thrombosis and Vascular Biology, 2003
    Co-Authors: Donald D. Heistad
    Abstract:

    When our editorship began in the spring of 1999, we summarized our goals: to publish high-quality papers, to provide timely review and publication, and to publish papers that would be of special interest to our readers. In this report, we will summarize progress toward these goals. In addition, we will summarize some new initiatives and thank several people for their help. The Editors rely greatly on reviewers to advise us about the scientific validity of conclusions in manuscripts. Novelty and importance of papers is very difficult to judge, and the editors also rely heavily on the advice of expert reviewers and the Editorial Board. One measure of importance in quality of papers is the impact factor. The latest available data (for 2001) indicate that the impact factor for Arteriosclerosis, Thrombosis, and Vascular Biology ( ATVB ) has increased substantially during the past year (from 5.1 to 5.8), and has increased from 3.9 to 5.8 during the three years of our editorship (Figure 1). In comparison with other journals in this area of research, ATVB continues to be extremely competitive. Figure 1. Impact factor. Recently, we have begun to track the “immediacy index,” which refers to the frequency of references to articles within the first year. The immediacy index has increased during the past several years (Figure 2). Figure 2. Immediacy index. One of our major goals is to provide expert, rapid reviews of manuscripts that are submitted to ATVB . The average time from receipt of new manuscripts to …

  • Progress Report, Arteriosclerosis, Thrombosis, and Vascular Biology
    Arteriosclerosis Thrombosis and Vascular Biology, 2002
    Co-Authors: Donald D. Heistad
    Abstract:

    The goal of ATVB is to rapidly publish the best work related to atherosclerosis, thrombosis, and Vascular Biology. We will describe briefly several developments toward that goal. The Institute for Scientific Research has placed all American Heart Association journals in the Peripheral Vascular Disease category. ATVB has maintained its ranking within this category as the leading journal in each of its areas of focus: atherosclerosis, thrombosis, and Vascular Biology. We recognize the many limitations of calculation of impact factor, but nevertheless, one of our goals is …

Rhian M. Touyz - One of the best experts on this subject based on the ideXlab platform.

  • Vascular Biology of ageing-Implications in hypertension.
    Journal of molecular and cellular cardiology, 2015
    Co-Authors: Adam Harvey, Augusto C. Montezano, Rhian M. Touyz
    Abstract:

    Ageing is associated with functional, structural and mechanical changes in arteries that closely resemble the Vascular alterations in hypertension. Characteristic features of large and small arteries that occur with ageing and during the development of hypertension include endothelial dysfunction, Vascular remodelling, inflammation, calcification and increased stiffness. Arterial changes in young hypertensive patients mimic those in old normotensive individuals. Hypertension accelerates and augments age-related Vascular remodelling and dysfunction, and ageing may impact on the severity of Vascular damage in hypertension, indicating close interactions between biological ageing and blood pressure elevation. Molecular and cellular mechanisms underlying Vascular alterations in ageing and hypertension are common and include aberrant signal transduction, oxidative stress and activation of pro-inflammatory and pro-fibrotic transcription factors. Strategies to suppress age-associated Vascular changes could ameliorate Vascular damage associated with hypertension. An overview on the Vascular Biology of ageing and hypertension is presented and novel molecular mechanisms contributing to these processes are discussed. The complex interaction between biological ageing and blood pressure elevation on the vasculature is highlighted. This article is part of a Special Issue entitled: CV Ageing.

  • reactive oxygen species and Vascular Biology implications in human hypertension
    Hypertension Research, 2011
    Co-Authors: Rhian M. Touyz, Ana M Briones
    Abstract:

    Increased Vascular production of reactive oxygen species (ROS; termed oxidative stress) has been implicated in various chronic diseases, including hypertension. Oxidative stress is both a cause and a consequence of hypertension. Although oxidative injury may not be the sole etiology, it amplifies blood pressure elevation in the presence of other pro-hypertensive factors. Oxidative stress is a multisystem phenomenon in hypertension and involves the heart, kidneys, nervous system, vessels and possibly the immune system. Compelling experimental and clinical evidence indicates the importance of the vasculature in the pathophysiology of hypertension and as such much emphasis has been placed on the (patho)Biology of ROS in the Vascular system. A major source for cardioVascular, renal and neural ROS is a family of non-phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox), including the prototypic Nox2 homolog-based NADPH oxidase, as well as other Noxes, such as Nox1 and Nox4. Nox-derived ROS is important in regulating endothelial function and Vascular tone. Oxidative stress is implicated in endothelial dysfunction, inflammation, hypertrophy, apoptosis, migration, fibrosis, angiogenesis and rarefaction, important processes involved in Vascular remodeling in hypertension. Despite a plethora of data implicating oxidative stress as a causative factor in experimental hypertension, findings in human hypertension are less conclusive. This review highlights the importance of ROS in Vascular Biology and focuses on the potential role of oxidative stress in human hypertension.

  • Vascular Biology of magnesium and its transporters in hypertension
    Magnesium Research, 2010
    Co-Authors: Alvaro Yogi, Glaucia E. Callera, Tayze T. Antunes, Rita C. Tostes, Rhian M. Touyz
    Abstract:

    Magnesium may influence blood pressure by modulating Vascular tone and structure through its effects on myriad biochemical reactions that control Vascular contraction/dilation, growth/apoptosis, differentiation and inflammation. Magnesium acts as a calcium channel antagonist, it stimulates production of vasodilator prostacyclins and nitric oxide and it alters Vascular responses to vasoconstrictor agents. Mammalian cells regulate Mg 2+ concentration through special transport systems that have only recently been characterized. Magnesium efflux occurs via Na 2+-dependent and Na 2+-independent pathways. Mg 2+ influx is controlled by recently cloned transporters including Mrs2p, SLC41A1, SLC41A2, ACDP2, MagT1, TRPM6 and TRPM7. Alterations in some of these systems may contribute to hypomagnesemia and intracellular Mg 2+ deficiency in hypertension and other cardioVascular pathologies. In particular, increased Mg 2+ efflux through dysregulation of the Vascular Na +/Mg 2+ exchanger and decreased Mg 2+ influx due to defective Vascular and renal TRPM6/7 expression/activity may be important in altered vasomotor tone and consequently in blood pressure regulation. The present review discusses the role of Mg 2+ in Vascular Biology and implications in hypertension and focuses on the putative transport systems that control magnesium homeostasis in the Vascular system. Much research is still needed to clarify the exact mechanisms of cardioVascular Mg 2+ regulation and the implications of aberrant cellular Mg 2+ transport and altered cation status in the pathogenesis of hypertension and other cardioVascular diseases.

  • Reactive oxygen species in Vascular Biology: implications in hypertension
    Histochemistry and cell biology, 2004
    Co-Authors: Rhian M. Touyz, Ernesto L. Schiffrin
    Abstract:

    Reactive oxygen species (ROS), including superoxide (*O2-), hydrogen peroxide (H2O2), and hydroxyl anion (OH-), and reactive nitrogen species, such as nitric oxide (NO) and peroxynitrite (ONOO-), are biologically important O2 derivatives that are increasingly recognized to be important in Vascular Biology through their oxidation/reduction (redox) potential. All Vascular cell types (endothelial cells, Vascular smooth muscle cells, and adventitial fibroblasts) produce ROS, primarily via cell membrane-associated NAD(P)H oxidase. Reactive oxygen species regulate Vascular function by modulating cell growth, apoptosis/anoikis, migration, inflammation, secretion, and extracellular matrix protein production. An imbalance in redox state where pro-oxidants overwhelm anti-oxidant capacity results in oxidative stress. Oxidative stress and associated oxidative damage are mediators of Vascular injury and inflammation in many cardioVascular diseases, including hypertension, hyperlipidemia, and diabetes. Increased generation of ROS has been demonstrated in experimental and human hypertension. Anti-oxidants and agents that interrupt NAD(P)H oxidase-driven *O2- production regress Vascular remodeling, improve endothelial function, reduce inflammation, and decrease blood pressure in hypertensive models. This experimental evidence has evoked considerable interest because of the possibilities that therapies targeted against reactive oxygen intermediates, by decreasing generation of ROS and/or by increasing availability of antioxidants, may be useful in minimizing Vascular injury and hypertensive end organ damage. The present chapter focuses on the importance of ROS in Vascular Biology and discusses the role of oxidative stress in Vascular damage in hypertension.

Stefanie Dimmeler - One of the best experts on this subject based on the ideXlab platform.

  • Long non-coding RNAs in Vascular Biology and disease.
    Vascular pharmacology, 2019
    Co-Authors: Nicolas Jaé, Andreas W. Heumüller, Youssef Fouani, Stefanie Dimmeler
    Abstract:

    The advent of deep sequencing technologies recently unraveled the complexity of the human genome: Although almost entirely transcribed, only a very minor part of our genome actually accounts for protein coding exons and most is considered non-coding. Among the non-coding transcripts, long non-coding RNAs (lncRNAs) constitute a rather heterogeneous group of linear as well as circular RNAs (circRNAs). LncRNAs act via multiple mechanisms and several lncRNAs were shown to be involved in Vascular development, growth and remodeling. For example, the lncRNAs PUNISHER, MALAT1, MEG3, and GATA6-AS regulate vessel formation in vivo, whereas lincRNA-p21 controls smooth muscle cell function and neointima formation. For several other lncRNAs (e.g. SENCR, SMILR, and HypERlnc) functional roles in smooth muscle cells/pericytes have been described in vitro. Less information is available with respect to the function of circRNAs. Here most studies report on expression profiles but some circRNAs (e.g. cANRIL or cZNF292) may also play critical roles in smooth muscle or endothelial cells in vitro. This review summarizes the current knowledge of lncRNA and circRNA functions in Vascular Biology and disease and discusses their potential use as biomarkers.

  • endothelial progenitor cells characterization and role in Vascular Biology
    Circulation Research, 2004
    Co-Authors: Carmen Urbich, Stefanie Dimmeler
    Abstract:

    Infusion of different hematopoietic stem cell populations and ex vivo expanded endothelial progenitor cells augments neoVascularization of tissue after ischemia and contributes to reendothelialization after endothelial injury, thereby, providing a novel therapeutic option. However, controversy exists with respect to the identification and the origin of endothelial progenitor cells. Overall, there is consensus that endothelial progenitor cells can derive from the bone marrow and that CD133/VEGFR2 cells represent a population with endothelial progenitor capacity. However, increasing evidence suggests that there are additional bone marrow-derived cell populations (eg, myeloid cells, “side population” cells, and mesenchymal cells) and non-bone marrow-derived cells, which also can give rise to endothelial cells. The characterization of the different progenitor cell populations and their functional properties are discussed. Mobilization and endothelial progenitor cell-mediated neoVascularization is critically regulated. Stimulatory (eg, statins and exercise) or inhibitory factors (risk factors for coronary artery disease) modulate progenitor cell levels and, thereby, affect the Vascular repair capacity. Moreover, recruitment and incorporation of endothelial progenitor cells requires a coordinated sequence of multistep adhesive and signaling events including adhesion and migration (eg, by integrins), chemoattraction (eg, by SDF-1/CXCR4), and finally the differentiation to endothelial cells. This review summarizes the mechanisms regulating endothelial progenitor cell-mediated neoVascularization and reendothelialization. This Review is part of a thematic series on Angiogenesis, which includes the following articles: Endothelial Progenitor Cells: Characterization and Role in Vascular Biology Bone Marrow–Derived Cells for Enhancing Collateral Development: Mechanisms, Animal Data, and Initial Clinical Experiences Arteriogenesis Innate Immunity and Angiogenesis Syndecans Growth Factors and Blood Vessels: Differentiation and Maturation Ralph Kelly Guest Editor

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