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Coronary Artery Disease: HELP
Articles by Susan S. Smyth
Based on 5 articles published since 2010
(Why 5 articles?)
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Between 2010 and 2020, Susan S. Smyth wrote the following 5 articles about Coronary Artery Disease.
 
+ Citations + Abstracts
1 Review Lysophospholipids in coronary artery and chronic ischemic heart disease. 2015

Abdel-Latif, Ahmed / Heron, Paula M / Morris, Andrew J / Smyth, Susan S. ·aDepartment of Veterans Affairs Medical Center bDivision of Cardiovascular Medicine, The Gill Heart Institute cUniversity of Kentucky, Lexington, Kentucky, USA. ·Curr Opin Lipidol · Pubmed #26270808.

ABSTRACT: PURPOSE OF REVIEW: The bioactive lysophospholipids, lysophosphatidic acid (LPA) and sphingosine 1 phosphate (S1P), have potent effects on blood and vascular cells. This review focuses their potential contributions to the development of atherosclerosis, acute complications such as acute myocardial infarction, and chronic ischemic cardiac damage. RECENT FINDINGS: Exciting recent developments have provided insight into the molecular underpinnings of LPA and S1P receptor signaling. New lines of evidence suggest roles for these pathways in the development of atherosclerosis. In experimental animal models, the production, signaling, and metabolism of LPA may be influenced by environmental factors in the diet that synergize to promote the progression of atherosclerotic vascular disease. This is supported by observations of human polymorphisms in the lysophospholipid-metabolizing enzyme PPAP2B, which are associated with risk of coronary artery disease and myocardial infarction. S1P signaling protects from myocardial damage that follows acute and chronic ischemia, both by direct effects on cardiomyocytes and through stem cell recruitment to ischemic tissue. SUMMARY: This review will suggest novel strategies to prevent the complications of coronary artery disease by targeting LPA production and signaling. Additionally, ways in which S1P signaling pathways may be harnessed to attenuate ischemia-induced cardiac dysfunction will be explored.

2 Review Arguing the case for the autotaxin-lysophosphatidic acid-lipid phosphate phosphatase 3-signaling nexus in the development and complications of atherosclerosis. 2014

Smyth, Susan S / Mueller, Paul / Yang, Fanmuyi / Brandon, J Anthony / Morris, Andrew J. ·From the Veterans Affairs Medical Center, Cardiovascular Medicine Service, Lexington, KY (S.S.S., A.J.M.) · and Division of Cardiovascular Medicine, Gill Heart Institute, University of Kentucky, Lexington, KY (S.S.S., P.M., F.Y., J.A.B., A.J.M.). ·Arterioscler Thromb Vasc Biol · Pubmed #24482375.

ABSTRACT: The structurally simple glycero- and sphingo-phospholipids, lysophosphatidic acid (LPA) and sphingosine-1-phosphate, serve as important receptor-active mediators that influence blood and vascular cell function and are positioned to influence the events that contribute to the progression and complications of atherosclerosis. Growing evidence from preclinical animal models has implicated LPA, LPA receptors, and key enzymes involved in LPA metabolism in pathophysiologic events that may underlie atherosclerotic vascular disease. These observations are supported by genetic analysis in humans implicating a lipid phosphate phosphatase as a novel risk factor for coronary artery disease. In this review, we summarize current understanding of LPA production, metabolism, and signaling as may be relevant for atherosclerotic and other vascular disease.

3 Article Coronary Artery Disease Risk-Associated 2019

Mueller, Paul A / Yang, Liping / Ubele, Margo / Mao, Guogen / Brandon, Jason / Vandra, Julia / Nichols, Timothy C / Escalante-Alcalde, Diana / Morris, Andrew J / Smyth, Susan S. ·From the Division of Cardiovascular Medicine, The Gill Heart & Vascular Institute, University of Kentucky, Lexington (P.A.M., L.Y., M.U., G.M., J.B., J.V., A.J.M., S.S.S.). · Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill (T.C.N.). · División de Neurociencias, Instituto de Fisiología, Celular Universidad Nacional Autónoma de México, Ciudad de México, CDMX (D.E.-A.). · Department of Veterans Affairs Medical Center, Lexington, KY (A.J.M., S.S.S.). ·Arterioscler Thromb Vasc Biol · Pubmed #31533471.

ABSTRACT: OBJECTIVE: Genome-wide association studies identified novel loci in CONCLUSIONS: Our results identify a novel lipid signaling pathway that regulates inflammation in the context of atherosclerosis and is not related to traditional risk factors. Pharmacological targeting of bioactive LPP3 substrates, including LPA, may offer an orthogonal approach to lipid-lowering drugs for mitigation of coronary artery disease risk.

4 Article Lipid-induced epigenomic changes in human macrophages identify a coronary artery disease-associated variant that regulates PPAP2B Expression through Altered C/EBP-beta binding. 2015

Reschen, Michael E / Gaulton, Kyle J / Lin, Da / Soilleux, Elizabeth J / Morris, Andrew J / Smyth, Susan S / O'Callaghan, Christopher A. ·Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, United Kingdom. · Nuffield Department of Clinical Laboratory Sciences, University of Oxford and Department of Cellular Pathology, John Radcliffe Hospital, Oxford, United Kingdom. · Division of Cardiovascular Medicine, The Gill Heart Institute, University of Kentucky, Lexington, Kentucky, United States of America; Department of Veterans Affairs Medical Center, Lexington, Kentucky, United States of America. ·PLoS Genet · Pubmed #25835000.

ABSTRACT: Genome-wide association studies (GWAS) have identified over 40 loci that affect risk of coronary artery disease (CAD) and the causal mechanisms at the majority of loci are unknown. Recent studies have suggested that many causal GWAS variants influence disease through altered transcriptional regulation in disease-relevant cell types. We explored changes in transcriptional regulation during a key pathophysiological event in CAD, the environmental lipid-induced transformation of macrophages to lipid-laden foam cells. We used a combination of open chromatin mapping with formaldehyde-assisted isolation of regulatory elements (FAIRE-seq) and enhancer and transcription factor mapping using chromatin immuno-precipitation (ChIP-seq) in primary human macrophages before and after exposure to atherogenic oxidized low-density lipoprotein (oxLDL), with resultant foam cell formation. OxLDL-induced foam cell formation was associated with changes in a subset of open chromatin and active enhancer sites that strongly correlated with expression changes of nearby genes. OxLDL-regulated enhancers were enriched for several transcription factors including C/EBP-beta, which has no previously documented role in foam cell formation. OxLDL exposure up-regulated C/EBP-beta expression and increased genomic binding events, most prominently around genes involved in inflammatory response pathways. Variants at CAD-associated loci were significantly and specifically enriched in the subset of chromatin sites altered by oxLDL exposure, including rs72664324 in an oxLDL-induced enhancer at the PPAP2B locus. OxLDL increased C/EBP beta binding to this site and C/EBP beta binding and enhancer activity were stronger with the protective A allele of rs72664324. In addition, expression of the PPAP2B protein product LPP3 was present in foam cells in human atherosclerotic plaques and oxLDL exposure up-regulated LPP3 in macrophages resulting in increased degradation of pro-inflammatory mediators. Our results demonstrate a genetic mechanism contributing to CAD risk at the PPAP2B locus and highlight the value of studying epigenetic changes in disease processes involving pathogenic environmental stimuli.

5 Article Spontaneous coronary thrombosis following thrombolytic therapy for acute cardiovascular accident and stroke: a case study. 2012

Wallace, Eric L / Smyth, Susan S. ·Division of Cardiovascular Medicine, The Gill Heart Institute, University of Kentucky, The Lexington VA Medical Center, 900 S. Limestone Street, 326 CTW Building, Lexington, KY 40536-0200, USA. eric.wallace@uky.edu ·J Thromb Thrombolysis · Pubmed #22684577.

ABSTRACT: Cardiac complications following stroke or acute cerebrovascular accidents (CVA) are common; however, many of these complications are asymptomatic and do not cause adverse cardiac effects. Symptomatic events (such as acute myocardial infarction after CVA) rarely occur and are often the result of an underlying cardiac embolic source, such as a left ventricular thrombus. We report a case of spontaneous coronary thrombosis following thrombolytic therapy for acute CVA, and discuss the implication that an underlying systemic pro-thrombotic state may predispose individuals to thrombosis in disparate vascular beds.