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Biology and Biochemistry

D-Index
50
Citations
10009
World Ranking
17564
National Ranking
1386

Overview

Joseph J. Boyle is affiliated with Imperial College London in the United Kingdom. Their research spans across the fields of Medicine and Biochemistry, Genetics and Molecular Biology, with 25 and 18 publications in these areas respectively. Subfields of study include Molecular Biology, Cardiology and Cardiovascular Medicine, Surgery, Pulmonary and Respiratory Medicine, and Pathology and Forensic Medicine.

The scientist's main research topics encompass congenital heart defects research, heme oxygenase-1 and carbon monoxide, cardiac fibrosis and remodeling, single-cell and spatial transcriptomics, viral infections and immunology research, cardiac ischemia and reperfusion, as well as cerebrovascular and carotid artery diseases.

Joseph J. Boyle's recent papers include the following:

  • Cells of the adult human heart, 2020, Nature
  • A Coumarin-Porphyrin FRET Break-Apart Probe for Heme Oxygenase-1, 2021, Journal of the American Chemical Society
  • Pleiotropic genetic architecture and novel loci for C-reactive protein levels, 2022, Nature Communications
  • Metformin directly suppresses atherosclerosis in normoglycaemic mice via haematopoietic adenosine monophosphate-activated protein kinase, 2020, Cardiovascular Research
  • Type 2 MI induced by a single high dose of isoproterenol in C57BL/6J mice triggers a persistent adaptive immune response against the heart, 2020, Journal of Cellular and Molecular Medicine

The frequent co-authors collaborating with Joseph J. Boyle are:

  • Nicholas J. Long
  • Edward R. H. Walter
  • Justin C. Mason
  • Luke Cave
  • Dorian O. Haskard

Joseph J. Boyle's work has been published mostly in the following venues:

  • bioRxiv (Cold Spring Harbor Laboratory)
  • Nature
  • Journal of the American Chemical Society
  • Nature Communications
  • Cardiovascular Research

Best Publications

  • Cells of the adult human heart.

    Monika Litviňuková;Monika Litviňuková;Carlos Talavera-López;Carlos Talavera-López;Henrike Maatz;Daniel Reichart;Daniel Reichart

  • Copy number polymorphism in Fcgr3 predisposes to glomerulonephritis in rats and humans

    Timothy J. Aitman;Rong Dong;Timothy J. Vyse;Penny J. Norsworthy

  • Macrophage activation in atherosclerosis: pathogenesis and pharmacology of plaque rupture.

    Boyle Jj

  • Coronary Intraplaque Hemorrhage Evokes a Novel Atheroprotective Macrophage Phenotype

    Joseph J. Boyle;Heather A. Harrington;Emma Piper;Kay Elderfield

  • Immunoglobulin M Is Required for Protection Against Atherosclerosis in Low-Density Lipoprotein Receptor–Deficient Mice

    Myles J. Lewis;Talat H. Malik;Michael R. Ehrenstein;Joseph J. Boyle

  • Tumor Necrosis Factor-α Promotes Macrophage-Induced Vascular Smooth Muscle Cell Apoptosis by Direct and Autocrine Mechanisms

    Joseph J. Boyle;Peter L. Weissberg;Martin R. Bennett

  • Linked Chromosome 16q13 Chemokines, Macrophage-Derived Chemokine, Fractalkine, and Thymus- and Activation-Regulated Chemokine, Are Expressed in Human Atherosclerotic Lesions

    David R. Greaves;Tomi Häkkinen;Andrew D. Lucas;Kate Liddiard

  • Specific C-Terminal Cleavage and Inactivation of Interleukin-8 by Invasive Disease Isolates of Streptococcus pyogenes

    Robert J. Edwards;Graham W. Taylor;Melissa Ferguson;Stephen Murray

  • EndoPDI, a Novel Protein-disulfide Isomerase-like Protein That Is Preferentially Expressed in Endothelial Cells Acts as a Stress Survival Factor

    Dianne C. Sullivan;Lucasz Huminiecki;John W. Moore;Joseph J. Boyle

  • Activating Transcription Factor 1 Directs Mhem Atheroprotective Macrophages Through Coordinated Iron Handling and Foam Cell Protection

    Joseph J. Boyle;Michael Johns;Theresa Kampfer;Theresa Kampfer;Aivi T. Nguyen

  • ASSOCIATION OF CORONARY PLAQUE RUPTURE AND ATHEROSCLEROTIC INFLAMMATION

    J. J. Boyle

  • Complement C1q reduces early atherosclerosis in low-density lipoprotein receptor-deficient mice.

    Vinay K. Bhatia;Sheng Yun;Sheng Yun;Viola Leung;Viola Leung;David C. Grimsditch

  • Cooperative Interactions Between RB and p53 Regulate Cell Proliferation, Cell Senescence, and Apoptosis in Human Vascular Smooth Muscle Cells From Atherosclerotic Plaques

    Martin R. Bennett;Kirsty Macdonald;Shiu Wan Chan;Joseph J. Boyle

  • Human Blood-Derived Macrophages Induce Apoptosis in Human Plaque-Derived Vascular Smooth Muscle Cells by Fas-Ligand/Fas Interactions

    Joseph J. Boyle;David E. Bowyer;Peter L. Weissberg;Martin R. Bennett

  • Heme Induces Heme Oxygenase 1 via Nrf2 Role in the Homeostatic Macrophage Response to Intraplaque Hemorrhage

    Joseph J. Boyle;Michael Johns;Jonathan Lo;Alessandra Chiodini

  • Mycobacterium tuberculosis Up-Regulates Matrix Metalloproteinase-1 Secretion from Human Airway Epithelial Cells via a p38 MAPK Switch

    Paul T. G. Elkington;Jenny E. Emerson;Laura D. C. Lopez-Pascua;Cecilia M. O’Kane

  • Human macrophage-induced vascular smooth muscle cell apoptosis requires NO enhancement of Fas/Fas-L interactions.

    Joseph J. Boyle;Peter L. Weissberg;Martin R. Bennett

  • Mycobacterium tuberculosis, but not vaccine BCG, specifically upregulates matrix metalloproteinase-1.

    Paul T. G. Elkington;Robert K. Nuttall;Joseph J. Boyle;Cecilia M. O'Kane

  • Vascular smooth muscle cell detachment from elastin and migration through elastic laminae is promoted by chondroitin sulfate-induced “shedding” of the 67-kDa cell surface elastin binding protein

    Aleksander Hinek;Jennifer Boyle;Marlene Rabinovitch

  • Apoptosis of vascular smooth muscle cells in atherosclerosis

    Martin R Bennett;Joseph J Boyle

Frequent Co-Authors

Dorian O. Haskard
Dorian O. Haskard Imperial College London
Paul C. Evans
Paul C. Evans Queen Mary University of London
Marina Botto
Marina Botto Imperial College London
David Carling
David Carling Imperial College London
Martin R. Bennett
Martin R. Bennett University of Cambridge
Jon S. Friedland
Jon S. Friedland St George's, University of London
Sheila E. Francis
Sheila E. Francis University of Sheffield
Paul M. Matthews
Paul M. Matthews Imperial College London
Christine E. Seidman
Christine E. Seidman Harvard University
Timothy J. Vyse
Timothy J. Vyse King's College London

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