Harnessing the Plasma Proteome to Mirror Current and Predict Future Cardiac Remodeling After Myocardial Infarction
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Michael E. Hall | M. Lindsey | Leah M. Cook | M. Hall | K. DeLeon-Pennell | Upendra Chalise | Shelby R. Konfrst | Jocelyn R Rodriguez-Paar | Mediha Becirovic-Agic | D. Anderson | Sharon D B de Morais | L. Cook | Elizabeth R. Flynn | Mediha Becirovic‐Agic | Catherine S Johnson | Catherine S. Johnson | Jocelyn R. Rodriguez-Paar
[1] F. Bengel,et al. Characterizing the transition from immune response to tissue repair after myocardial infarction by multiparametric imaging , 2022, Basic Research in Cardiology.
[2] M. Lindsey,et al. Macrophages secrete murinoglobulin-1 and galectin-3 to regulate neutrophil degranulation after myocardial infarction , 2022, Molecular omics.
[3] Michael E. Hall,et al. Faster skin wound healing predicts survival after myocardial infarction , 2022, American journal of physiology. Heart and circulatory physiology.
[4] M. Lindsey,et al. S100A9 is a functional effector of infarct wall thinning after myocardial infarction , 2021, American journal of physiology. Heart and circulatory physiology.
[5] M. Lindsey,et al. Neutrophil crosstalk during cardiac wound healing after myocardial infarction. , 2021, Current opinion in physiology.
[6] P. Pagliaro,et al. Regulation of STAT3 and its role in cardioprotection by conditioning: focus on non-genomic roles targeting mitochondrial function , 2021, Basic Research in Cardiology.
[7] Min Zhang,et al. Regulatory B cells improve ventricular remodeling after myocardial infarction by modulating monocyte migration , 2021, Basic Research in Cardiology.
[8] M. Lindsey,et al. Reperfused vs. Non-reperfused Myocardial Infarction: When to Use Which Model. , 2021, American journal of physiology. Heart and circulatory physiology.
[9] F. Montecucco,et al. Cytokines as therapeutic targets for cardio- and cerebrovascular diseases , 2021, Basic Research in Cardiology.
[10] M. Lindsey,et al. Infarct in the Heart: What’s MMP-9 Got to Do with It? , 2021, Biomolecules.
[11] Kathleen M. Jagodnik,et al. Gene Set Knowledge Discovery with Enrichr , 2021, Current protocols.
[12] K. Peter,et al. Alarmin-activated B cells accelerate murine atherosclerosis after myocardial infarction via plasma cell-immunoglobulin-dependent mechanisms. , 2020, European heart journal.
[13] M. Lindsey,et al. Neutrophil signaling during myocardial infarction wound repair. , 2020, Cellular signalling.
[14] M. Lindsey,et al. Exogenous IL-4 shuts off pro-inflammation in neutrophils while stimulating anti-inflammation in macrophages to induce neutrophil phagocytosis following myocardial infarction , 2020, Journal of molecular and cellular cardiology.
[15] M. Lindsey,et al. Cardiac Fibroblast Activation during Myocardial Infarction Wound Healing: Fibroblast polarization after MI. , 2020, Matrix biology : journal of the International Society for Matrix Biology.
[16] O. Akgul,et al. The prognostic value of elevated matrix metalloproteinase-9 in patients undergoing primary percutaneous coronary intervention for ST-elevation myocardial infarction: A two-year prospective study , 2020, Revista Portuguesa de Cardiologia (English Edition).
[17] M. Lindsey,et al. The compendium of matrix metalloproteinase expression in the left ventricle of mice following myocardial infarction. , 2020, American journal of physiology. Heart and circulatory physiology.
[18] Jianfang Liu,et al. The expression of interleukin-25 increases in human coronary artery disease and is associated with the severity of coronary stenosis , 2020, Anatolian journal of cardiology.
[19] Anindita Das,et al. STAT3-miR-17/20 Signaling Axis Plays a Critical Role in Attenuating Myocardial Infarction following Rapamycin Treatment in Diabetic mice. , 2019, Cardiovascular research.
[20] M. Lindsey,et al. Understanding the mechanisms that determine extracellular matrix remodeling in the infarcted myocardium. , 2019, Biochemical Society transactions.
[21] M. Lindsey,et al. Neutrophil proteome shifts over the myocardial infarction time continuum , 2019, Basic Research in Cardiology.
[22] M. Carli,et al. Cardiovascular Volume Reserve in Patients with Heart Failure and Reduced Ejection Fraction , 2019, Journal of Cardiovascular Translational Research.
[23] Michael E. Hall,et al. Identifying the molecular and cellular signature of cardiac dilation following myocardial infarction. , 2019, Biochimica et biophysica acta. Molecular basis of disease.
[24] S. Feinstein,et al. Reciprocal Multifaceted Interaction Between HDL (High-Density Lipoprotein) and Myocardial Infarction. , 2019, Arteriosclerosis, thrombosis, and vascular biology.
[25] Pei Yang,et al. E3-ubiquitin ligase TRIM6 aggravates myocardial ischemia/reperfusion injury via promoting STAT1-dependent cardiomyocyte apoptosis , 2019, Aging.
[26] M. Lindsey,et al. Fibroblast polarization over the myocardial infarction time continuum shifts roles from inflammation to angiogenesis , 2019, Basic Research in Cardiology.
[27] Liu Liu,et al. HDAC inhibitor valproic acid protects heart function through Foxm1 pathway after acute myocardial infarction , 2018, EBioMedicine.
[28] K. Fukuda,et al. IL (Interleukin)-10–STAT3–Galectin-3 Axis Is Essential for Osteopontin-Producing Reparative Macrophage Polarization After Myocardial Infarction , 2018, Circulation.
[29] Abdullah Kaplan,et al. The Mouse Heart Attack Research Tool 1.0 database. , 2018, American journal of physiology. Heart and circulatory physiology.
[30] Michael E. Hall,et al. Exogenous CXCL4 infusion inhibits macrophage phagocytosis by limiting CD36 signalling to enhance post-myocardial infarction cardiac dilation and mortality , 2018, Cardiovascular research.
[31] M. Lindsey,et al. Statistical considerations in reporting cardiovascular research. , 2018, American journal of physiology. Heart and circulatory physiology.
[32] A. Mebazaa,et al. Plasma levels of heart failure biomarkers are primarily a reflection of extracardiac production , 2018, Theranostics.
[33] M. Lindsey,et al. Mapping macrophage polarization over the myocardial infarction time continuum , 2018, Basic Research in Cardiology.
[34] Hailing Yang,et al. Identification of Potential Molecular Mechanisms and Candidate Genes Involved in The Acute Phase of Myocardial Infarction , 2018, Cell journal.
[35] Steven P Jones,et al. Guidelines for experimental models of myocardial ischemia and infarction , 2018, American journal of physiology. Heart and circulatory physiology.
[36] M. Lindsey,et al. Guidelines for authors and reviewers on antibody use in physiology studies , 2018, American journal of physiology. Heart and circulatory physiology.
[37] M. Lindsey,et al. Guidelines for measuring cardiac physiology in mice , 2018, American journal of physiology. Heart and circulatory physiology.
[38] M. Brizzi,et al. Empagliflozin Limits Myocardial Infarction in Vivo and Cell Death in Vitro: Role of STAT3, Mitochondria, and Redox Aspects , 2017, Front. Physiol..
[39] S. Halvorsen,et al. MMP-9 and Its Regulators TIMP-1 and EMMPRIN in Patients with Acute ST-Elevation Myocardial Infarction: A NORDISTEMI Substudy , 2017, Cardiology.
[40] Xuemei Du,et al. IL-25 blockade inhibits metastasis in breast cancer , 2016, Protein & Cell.
[41] S. Prabhu,et al. The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis. , 2016, Circulation research.
[42] Andrew D. Rouillard,et al. Enrichr: a comprehensive gene set enrichment analysis web server 2016 update , 2016, Nucleic Acids Res..
[43] A. R. van der Velde,et al. Galectin-3 and post-myocardial infarction cardiac remodeling. , 2015, European journal of pharmacology.
[44] D. Tsiantoulas,et al. Targeting B cells in atherosclerosis: closing the gap from bench to bedside. , 2015, Arteriosclerosis, thrombosis, and vascular biology.
[45] H. Björkbacka,et al. IL-25 Inhibits Atherosclerosis Development in Apolipoprotein E Deficient Mice , 2015, PloS one.
[46] W. Abraham,et al. Novel Non-pharmacological Approaches to Heart Failure , 2014, Journal of Cardiovascular Translational Research.
[47] D. Tsiantoulas,et al. B lymphocytes trigger monocyte mobilization and impair heart function after acute myocardial infarction , 2013, Nature Medicine.
[48] M. Lindsey,et al. Matrix metalloproteinase (MMP)-9: a proximal biomarker for cardiac remodeling and a distal biomarker for inflammation. , 2013, Pharmacology & therapeutics.
[49] D. Mann,et al. Positioning of Inflammatory Biomarkers in the Heart Failure Landscape , 2013, Journal of Cardiovascular Translational Research.
[50] T. Costantino,et al. Neutrophil to lymphocyte ratio and cardiovascular diseases: a review , 2013, Expert review of cardiovascular therapy.
[51] Y. Arbel,et al. Neutrophil/lymphocyte ratio is related to the severity of coronary artery disease and clinical outcome in patients undergoing angiography. , 2012, Atherosclerosis.
[52] Dinender K Singla,et al. Overexpression of TIMP-1 in Embryonic Stem Cells Attenuates Adverse Cardiac Remodeling following Myocardial Infarction , 2012, Cell transplantation.
[53] R. Knight,et al. STAT1 deficiency in the heart protects against myocardial infarction by enhancing autophagy , 2012, Journal of cellular and molecular medicine.
[54] P. Armstrong,et al. Pattern of liver enzyme elevations in acute ST-elevation myocardial infarction , 2012, Coronary artery disease.
[55] T. Kalin,et al. Expression of Foxm1 Transcription Factor in Cardiomyocytes Is Required for Myocardial Development , 2011, PloS one.
[56] R. Vasan,et al. Biomarkers of Extracellular Matrix Metabolism (MMP-9 and TIMP-1) and Risk of Stroke, Myocardial Infarction, and Cause-Specific Mortality: Cohort Study , 2011, PloS one.
[57] C. Corrigan,et al. T-helper cell type 2 (Th2) memory T cell-potentiating cytokine IL-25 has the potential to promote angiogenesis in asthma , 2011, Proceedings of the National Academy of Sciences.
[58] P. Schwarz,et al. The iron-regulatory peptide hepcidin is upregulated in the ischemic and in the remote myocardium after myocardial infarction , 2010, Peptides.
[59] J. Gardner,et al. Estrogen improves TIMP-MMP balance and collagen distribution in volume-overloaded hearts of ovariectomized females. , 2010, American journal of physiology. Regulatory, integrative and comparative physiology.
[60] L. Ng,et al. Biomarkers in acute myocardial infarction , 2010, BMC medicine.
[61] J. V. van Engelshoven,et al. Leukocyte Counts, Myeloperoxidase, and Pregnancy-Associated Plasma Protein A as Biomarkers for Cardiovascular Disease: Towards a Multi-Biomarker Approach , 2010, International journal of vascular medicine.
[62] John S. Hill,et al. Myeloperoxidase and C-reactive protein have combined utility for long-term prediction of cardiovascular mortality after coronary angiography. , 2010, Journal of the American College of Cardiology.
[63] Adelaide M. Arruda-Olson,et al. Neutrophilia Predicts Death and Heart Failure After Myocardial Infarction: A Community-Based Study , 2009, Circulation. Cardiovascular quality and outcomes.
[64] P. Scheffer,et al. Myeloperoxidase: a useful biomarker for cardiovascular disease risk stratification? , 2009, Clinical chemistry.
[65] Raj Kishore,et al. IL-10 Inhibits Inflammation and Attenuates Left Ventricular Remodeling After Myocardial Infarction via Activation of STAT3 and Suppression of HuR , 2009, Circulation research.
[66] I. Holme,et al. Haptoglobin and risk of myocardial infarction, stroke, and congestive heart failure in 342,125 men and women in the Apolipoprotein MOrtality RISk study (AMORIS) , 2009, Annals of medicine.
[67] N. Samani,et al. Plasma tissue inhibitor of metalloproteinase-1 and matrix metalloproteinase-9: novel indicators of left ventricular remodelling and prognosis after acute myocardial infarction. , 2008, European heart journal.
[68] V. Cameron,et al. Plasma concentrations of myeloperoxidase predict mortality after myocardial infarction. , 2007, Journal of the American College of Cardiology.
[69] Leong L Ng,et al. Plasma matrix metalloproteinase-9 and left ventricular remodelling after acute myocardial infarction in man: a prospective cohort study. , 2007, European heart journal.
[70] A. Larsson,et al. Apolipoprotein A1 is a stronger prognostic marker than are HDL and LDL cholesterol for cardiovascular disease and mortality in elderly men. , 2006, The journals of gerontology. Series A, Biological sciences and medical sciences.
[71] Peipei Ping,et al. Cardiovascular proteomics: tools to develop novel biomarkers and potential applications. , 2006, Journal of the American College of Cardiology.
[72] S. Hazen,et al. Abstract 601: Haptoglobin Genotype Determines Myocardial Infarct Size in Diabetic Mice , 2006 .
[73] V. Chopra,et al. Tissue inhibitor of metalloproteinase-1 (TIMP-1) is an independent predictor of all-cause mortality, cardiac mortality, and myocardial infarction. , 2006, American heart journal.
[74] I. Holme,et al. High apolipoprotein B, low apolipoprotein A-I, and improvement in the prediction of fatal myocardial infarction (AMORIS study): a prospective study , 2001, The Lancet.
[75] T. Iwasaka,et al. Evidence for infection with Helicobacter pylori in patients with acute myocardial infarction. , 2001, Clinica chimica acta; international journal of clinical chemistry.
[76] M. Steffen,et al. Systemic acute‐phase reactants, C‐reactive protein and haptoglobin, in adult periodontitis , 1997, Clinical and experimental immunology.
[77] Andrew N. Rowan. Guide for the Care and Use of Laboratory Animals , 1996 .
[78] S. Tyagi,et al. Serum haptoglobin in cases of ischemic heart diseases. , 1980, Japanese heart journal.
[79] C. Binder,et al. ATVB IN FOCUS: Clinically Available Immunotherapies: Expected Impact on Cardiovascular Disease , 2019 .
[80] M. Borggrefe,et al. High plasma levels of tissue inhibitor of metalloproteinase-1 (TIMP-1) and interleukin-8 (IL-8) characterize patients prone to ventricular fibrillation complicating myocardial infarction , 2007, Clinical chemistry and laboratory medicine.
[81] P. Puddu,et al. Increased serum IgA levels in subjects with previous myocardial infarction or other major ischemic events. , 1993, Cardiology.