• Disease
  • Myocardial
  • Myocardial Infarction
  • Nikolaos Georgios Frangogiannis
  • Nikolaos Georgios Frangogiannis

    Nikolaos Georgios Frangogiannis


    Prominent publications by Nikolaos Georgios Frangogiannis

    KOL Index score: 14277

    BACKGROUND: Neutrophil-induced cardiomyocyte injury requires the expression of myocyte intercellular adhesion molecule (ICAM)-1 and ICAM-1-CD11b/CD18 adhesion. We have previously demonstrated interleukin (IL)-6 activity in postischemic cardiac lymph; IL-6 is the primary stimulus for myocyte ICAM- 1 induction. Furthermore, we found that induction of IL-6 mRNA occurred very early on reperfusion of the infarcted myocardium. We hypothesized that the release of a preformed upstream cytokine ...

    Also Ranks for: Cardiac Mast |  cytokine cascade |  canine myocardial |  ischemic myocardium |  induction il6
    KOL Index score: 13843

    Heart failure with preserved ejection fraction (HFpEF) is caused, or exacerbated by, a wide range of extracardiac conditions. Diabetes, obesity, and metabolic dysfunction are associated with a unique HFpEF phenotype, characterized by inflammation, cardiac fibrosis, and microvascular dysfunction. Development of new therapies for HFpEF is hampered by the absence of reliable animal models. The leptin-resistant db/ db mouse has been extensively studied as a model of diabetes-associated ...

    Also Ranks for: Mouse Model |  db mice |  preserved ejection |  heart failure |  ventricular function
    KOL Index score: 13050

    BACKGROUND: Myocardial infarction is associated with an intense inflammatory reaction leading to healing and scar formation. Because mast cells are a significant source of fibrogenic factors, we investigated mast cell accumulation and regulation of stem cell factor (SCF), a potent growth and tactic factor for mast cells, in the healing myocardium.

    METHODS AND RESULTS: Using a canine model of myocardial ischemia and reperfusion, we demonstrated a striking increase of mast cell numbers ...

    Also Ranks for: Mast Cell |  myocardial ischemia |  collagen deposition |  factor scf |  canine model
    KOL Index score: 12187

    OBJECTIVES: This study sought to examine the role of platelet-derived growth factor (PDGF) signaling in healing myocardial infarcts.

    BACKGROUND: Platelet-derived growth factor isoforms exert potent fibrogenic effects through interactions with PDGF receptor (PDGFR)-alpha and PDGFR-beta. In addition, PDGFR-beta signaling mediates coating of developing vessels with mural cells, leading to the formation of a mature vasculature. We hypothesized that PDGFR activation may regulate fibrosis and ...

    Also Ranks for: Growth Factor |  platelet derived |  healing myocardial |  vascular maturation |  collagen deposition
    KOL Index score: 11856

    AIMS: The CXC chemokine CXCL10 is up-regulated in the infarcted myocardium and limits cardiac fibrosis by inhibiting growth factor-mediated fibroblast migration. CXCL10 signals by binding to its receptor CXCR3; however, recently CXCR3-independent CXCL10 actions have been suggested. Our study explores the role of CXCR3 signalling in myocardial infarction and investigates its involvement in mediating the anti-fibrotic effects of CXCL10.

    METHODS AND RESULTS: Wild-type and CXCR3 null mice ...

    Also Ranks for: Cardiac Fibroblasts |  chemokine cxcl10 |  myocardial infarction |  infarcted myocardium |  antifibrotic effects
    KOL Index score: 11711

    Myocardial TGF-β expression is upregulated in experimental models of myocardial infarction and cardiac hypertrophy, and in patients with dilated or hypertrophic cardiomyopathy. Through its effects on cardiomyocytes, mesenchymal and immune cells, TGF-β plays an important role in the pathogenesis of cardiac remodeling and fibrosis. TGF-β overexpression in the mouse heart is associated with fibrosis and hypertrophy. Endogenous TGF-β plays an important role in the pathogenesis of cardiac ...

    Also Ranks for: Cardiac Remodeling |  β signaling |  transforming growth factor |  patients heart failure |  fibrosis hypertrophy
    KOL Index score: 11707

    One of the major therapeutic goals of modern cardiology is to design strategies aimed at minimizing myocardial necrosis and optimizing cardiac repair following myocardial infarction. However, a sound understanding of the biology is necessary before a specific intervention is pursued on a therapeutic basis. This review summarizes our current understanding of the cellular and molecular mechanisms regulating the inflammatory response following myocardial ischemia and reperfusion. Myocardial ...

    Also Ranks for: Myocardial Infarction |  inflammatory response |  cardiac repair |  neutrophil infiltration |  complement activation
    KOL Index score: 11651

    BACKGROUND: Previous work from our laboratory demonstrated that interleukin (IL)-6 plays a potentially critical role in postreperfusion myocardial injury and is the major cytokine responsible for induction of intracellular adhesion molecule (ICAM)-1 on cardiac myocytes during reperfusion. Myocyte ICAM-1 induction is necessary for neutrophil-associated myocyte injury. We have previously demonstrated the induction of IL-6 in the ischemic myocardium, and the current study addresses the ...

    Also Ranks for: Cardiac Myocytes |  border zone |  mrna expression |  induction il6 |  tumor necrosis factoralpha
    KOL Index score: 11512

    RATIONALE: Cardiovascular physiology and pathophysiology vary dramatically over the course of the day. For example, myocardial infarction onset occurs with greater incidence during the early morning hours in humans. However, whether myocardial infarction tolerance exhibits a time-of-day dependence is unknown.

    OBJECTIVE: To investigate whether time of day of an ischemic insult influences clinically relevant outcomes in mice.

    METHODS AND RESULTS: Wild-type mice were subjected to ...

    Also Ranks for: Time Day |  ischemia reperfusion |  synthase kinase |  transcription factors |  male mice mice
    KOL Index score: 11391

    TGF-βs regulate fibroblast responses, by activating Smad2 or Smad3 signaling, or via Smad-independent pathways. We have previously demonstrated that myofibroblast-specific Smad3 is critically implicated in repair of the infarcted heart. However, the role of fibroblast Smad2 in myocardial infarction remains unknown. This study investigates the role of myofibroblast-specific Smad2 signaling in myocardial infarction, and explores the mechanisms responsible for the distinct effects of Smad2 ...

    Also Ranks for: Smad2 Smad3 |  infarcted heart |  myocardial infarction |  coronary occlusion |  mice knockout
    KOL Index score: 11323

    BACKGROUND: There are currently no data on the accuracy of intravenous myocardial contrast echocardiography (MCE) in detecting myocardial hibernation in man and its comparative accuracy to dobutamine echocardiography (DE) or thallium 201 (Tl(201)) scintigraphy.

    METHODS AND RESULTS: Twenty patients with coronary artery disease and ventricular dysfunction underwent MCE 1 to 5 days before bypass surgery and repeat echocardiography at 3 to 4 months. Patients also underwent DE (n=18) and ...

    Also Ranks for: Hibernating Myocardium |  myocardial contrast |  recovery function |  contractile reserve |  quantitative intravenous
    KOL Index score: 11216

    Cardiac myofibroblasts play an important role in myocardial remodeling. Although α-smooth muscle actin (α-SMA) expression is the hallmark of mature myofibroblasts, its role in regulating fibroblast function remains poorly understood. We explore the effects of the matrix environment in modulating cardiac fibroblast phenotype, and we investigate the role of α-SMA in fibroblast function using loss- and gain-of-function approaches. In murine myocardial infarction, infiltration of the infarct ...

    Also Ranks for: Α Sma |  matrix contraction |  smooth muscle |  fibroblast function |  myocardial remodeling
    KOL Index score: 11047

    BACKGROUND: Matricellular proteins are extracellular matrix proteins that do not contribute directly to tissue integrity but are capable of modulating cell function. We hypothesized that the matricellular protein thrombospondin (TSP)-1, a potent inhibitor of angiogenesis and activator of transforming growth factor (TGF-beta), is induced in healing myocardial infarcts and plays a role in suppressing the postinfarction inflammatory response, inhibiting local angiogenesis, and limiting ...

    Also Ranks for: Myocardial Infarcts |  granulation tissue |  infarct border zone |  tsp1 mice |  matricellular proteins
    KOL Index score: 10984

    Myocardial infarction is associated with the rapid induction of mononuclear cell chemoattractants that promote monocyte infiltration into the injured area. Monocyte-to-macrophage differentiation and macrophage proliferation allow a long survival of monocytic cells, critical for effective healing of the infarct. In a canine infarction-reperfusion model, newly recruited myeloid leukocytes were markedly augmented during early reperfusion (5-72 h). By 7 days, the number of newly recruited ...

    Also Ranks for: Endothelial Cell |  myocardial infarcts |  macrophage proliferation |  stimulating factor |  healing infarct
    KOL Index score: 10884

    The β-galactoside-binding animal lectin galectin-3 is predominantly expressed by activated macrophages and is a promising biomarker for patients with heart failure. Galectin-3 regulates inflammatory and fibrotic responses; however, its role in cardiac remodeling remains unclear. We hypothesized that galectin-3 may be up-regulated in the pressure-overloaded myocardium and regulate hypertrophy and fibrosis. In normal mouse myocardium, galectin-3 was constitutively expressed in macrophages ...

    Also Ranks for: Cardiac Fibrosis |  hypertrophic response |  transverse aortic constriction |  overloaded heart |  survival dysfunction


    Nikolaos Georgios Frangogiannis: Influence Statistics

    Sample of concepts for which Nikolaos Georgios Frangogiannis is among the top experts in the world.
    Concept World rank
    infarcted myocardium immune #1
    recruitment healing #1
    pathophysiologic stratification #1
    heart failure il1 #1
    function proinflammatory environment #1
    infarct angiogenesis #1
    multiple suppressive pathways #1
    infarcted area tissue #1
    myocardial ischemia myocytes #1
    specific smad3 #1
    suppressive mononuclear cells #1
    cardiac pathologic conditions #1
    mechanisms fibroblast activation #1
    contribution cardiac dysfunction #1
    reparative myofibroblasts #1
    endogenous molecular signals #1
    modest transient reduction #1
    decreased dilative remodeling #1
    mac3 mac2 #1
    healing mouse infarcts #1
    myocardial ng2 pericytes #1
    sudden necrosis #1
    tregs infarcted myocardium #1
    tgfβ deactivates #1
    repair infarcted heart #1
    emerging concepts fibroblasts #1
    healing cardiac #1
    fibroblastspecific smad3 smad2 #1
    highmagnitude effects #1
    remodeling senescent #1
    expansion fibroblasts #1
    contraction αsma expression #1
    infarction inflammatory #1
    role smad pathways #1
    hypertrophic response survival #1
    infarction myofibroblasts #1
    infarcted il1ri #1
    ventricular disease study #1
    chemokines cardiac #1
    cellspecific approaches #1
    aging cardiac fibrosis #1
    modulating fibroblast #1
    fibrotic response obesity #1
    postinfarction inflammatory #1
    linked collagenous matrix #1
    proinflammatory gene synthesis #1
    chronic fibrogenic actions #1
    documentation rupture #1
    undergo myofibroblast #1
    null infarcts #1

    Key People For Myocardial Infarction

    Top KOLs in the world
    Braunwald Braunwald
    myocardial infarction heart failure atrial fibrillation
    Robert M Califf
    myocardial infarction thrombolytic therapy heart failure
    Frans J J Van de Werf
    myocardial infarction acute coronary thrombolytic therapy
    Eric J Topol
    myocardial infarction thrombolytic therapy coronary angioplasty
    Christian Wilhelm Hamm
    myocardial infarction aortic valve acute coronary syndromes
    Harlan M Krumholz
    heart failure united states acute myocardial infarction

    Nikolaos Georgios Frangogiannis:Expert Impact

    Concepts for whichNikolaos Georgios Frangogiannishas direct influence:Myocardial infarction,  Cardiac fibrosis,  Mast cells,  Infarcted myocardium,  Heart failure,  Extracellular matrix,  Myocardial ischemia,  Infarcted heart.

    Nikolaos Georgios Frangogiannis:KOL impact

    Concepts related to the work of other authors for whichfor which Nikolaos Georgios Frangogiannis has influence:Myocardial infarction,  Heart failure,  Cardiac fibrosis,  Reperfusion injury,  Extracellular matrix,  Oxidative stress,  Growth factor.



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    The Wilf Family Cardiovascular Research Institute, Department of Medicine (Cardiology), Albert Einstein College of Medicine, Bronx, NY, United States of America. Electronic address: nikolaos.frangogiannis@einsteinmed.edu. | The Wilf Family Cardiovasc