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  1. Article ; Online: Response by Frangogiannis to Letter Regarding Article, "Cardiac Pericytes Acquire a Fibrogenic Phenotype and Contribute to Vascular Maturation After Myocardial Infarction".

    Frangogiannis, Nikolaos G

    Circulation

    2024  Volume 149, Issue 12, Page(s) e962–e963

    MeSH term(s) Humans ; Pericytes ; Myocardial Infarction ; Heart ; Phenotype
    Language English
    Publishing date 2024-03-18
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.123.068236
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The fate and role of the pericytes in myocardial diseases.

    Frangogiannis, Nikolaos G

    European journal of clinical investigation

    2024  , Page(s) e14204

    Abstract: The adult mammalian heart contains a large population of pericytes that play important roles in homeostasis and disease. In the normal heart, pericytes regulate microvascular permeability and flow. Myocardial diseases are associated with marked ... ...

    Abstract The adult mammalian heart contains a large population of pericytes that play important roles in homeostasis and disease. In the normal heart, pericytes regulate microvascular permeability and flow. Myocardial diseases are associated with marked alterations in pericyte phenotype and function. This review manuscript discusses the role of pericytes in cardiac homeostasis and disease. Following myocardial infarction (MI), cardiac pericytes participate in all phases of cardiac repair. During the inflammatory phase, pericytes may secrete cytokines and chemokines and may regulate leukocyte trafficking, through formation of intercellular gaps that serve as exit points for inflammatory cells. Moreover, pericyte contraction induces microvascular constriction, contributing to the pathogenesis of 'no-reflow' in ischemia and reperfusion. During the proliferative phase, pericytes are activated by growth factors, such as transforming growth factor (TGF)-β and contribute to fibrosis, predominantly through secretion of fibrogenic mediators. A fraction of pericytes acquires fibroblast identity but contributes only to a small percentage of infarct fibroblasts and myofibroblasts. As the scar matures, pericytes form a coat around infarct neovessels, promoting stabilization of the vasculature. Pericytes may also be involved in the pathogenesis of chronic heart failure, by regulating inflammation, fibrosis, angiogenesis and myocardial perfusion. Pericytes are also important targets of viral infections (such as SARS-CoV2) and may be implicated in the pathogenesis of cardiac complications of COVID19. Considering their role in myocardial inflammation, fibrosis and angiogenesis, pericytes may be promising therapeutic targets in myocardial disease.
    Language English
    Publishing date 2024-04-08
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 186196-7
    ISSN 1365-2362 ; 0014-2972 ; 0960-135X
    ISSN (online) 1365-2362
    ISSN 0014-2972 ; 0960-135X
    DOI 10.1111/eci.14204
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  3. Article ; Online: TGF-β as a therapeutic target in the infarcted and failing heart: cellular mechanisms, challenges, and opportunities.

    Frangogiannis, Nikolaos G

    Expert opinion on therapeutic targets

    2024  Volume 28, Issue 1-2, Page(s) 45–56

    Abstract: Introduction: Myocardial fibrosis accompanies most cardiac conditions and can be reparative or maladaptive. Transforming Growth Factor (TGF)-β is a potent fibrogenic mediator, involved in repair, remodeling, and fibrosis of the injured heart.: Areas ... ...

    Abstract Introduction: Myocardial fibrosis accompanies most cardiac conditions and can be reparative or maladaptive. Transforming Growth Factor (TGF)-β is a potent fibrogenic mediator, involved in repair, remodeling, and fibrosis of the injured heart.
    Areas covered: This review manuscript discusses the role of TGF-β in heart failure focusing on cellular mechanisms and therapeutic implications. TGF-β is activated in infarcted, remodeling and failing hearts. In addition to its fibrogenic actions, TGF-β has a broad range of effects on cardiomyocytes, immune, and vascular cells that may have both protective and detrimental consequences. TGF-β-mediated effects on macrophages promote anti-inflammatory transition, whereas actions on fibroblasts mediate reparative scar formation and effects on pericytes are involved in maturation of infarct neovessels. On the other hand, TGF-β actions on cardiomyocytes promote adverse remodeling, and prolonged activation of TGF-β signaling in fibroblasts stimulates progression of fibrosis and heart failure.
    Expert opinion: Understanding of the cell-specific actions of TGF-β is necessary to design therapeutic strategies in patients with myocardial disease. Moreover, to implement therapeutic interventions in the heterogeneous population of heart failure patients, mechanism-driven classification of both HFrEF and HFpEF patients is needed. Heart failure patients with prolonged or overactive fibrogenic TGF-β responses may benefit from cautious TGF-β inhibition.
    MeSH term(s) Humans ; Heart Failure/drug therapy ; Transforming Growth Factor beta/metabolism ; Stroke Volume ; Myocardial Infarction/therapy ; Fibroblasts/metabolism ; Fibrosis ; Myocardium/pathology
    Chemical Substances Transforming Growth Factor beta
    Language English
    Publishing date 2024-02-19
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2055208-7
    ISSN 1744-7631 ; 1472-8222
    ISSN (online) 1744-7631
    ISSN 1472-8222
    DOI 10.1080/14728222.2024.2316735
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: The Many Faces of NLRs in Macrophage Biology.

    Frangogiannis, Nikolaos G

    JACC. Basic to translational science

    2023  Volume 8, Issue 5, Page(s) 497–500

    Language English
    Publishing date 2023-05-22
    Publishing country United States
    Document type Editorial
    ISSN 2452-302X
    ISSN (online) 2452-302X
    DOI 10.1016/j.jacbts.2023.02.004
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  5. Article ; Online: Fibroblasts, myofibroblasts and cardiac arrhythmias.

    Frangogiannis, Nikolaos G

    The journal of cardiovascular aging

    2023  Volume 3, Issue 4

    Language English
    Publishing date 2023-10-25
    Publishing country United States
    Document type Journal Article ; Comment
    ISSN 2768-5993
    ISSN (online) 2768-5993
    DOI 10.20517/jca.2023.37
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  6. Article ; Online: Targeting galectin-3 in myocardial infarction: a unique opportunity for biomarker-guided therapy.

    Frangogiannis, Nikolaos G

    Cardiovascular research

    2023  Volume 119, Issue 15, Page(s) 2495–2496

    MeSH term(s) Humans ; Galectin 3 ; Myocardial Infarction/diagnosis ; Myocardial Infarction/drug therapy ; Biomarkers ; Fibrosis
    Chemical Substances Galectin 3 ; Biomarkers
    Language English
    Publishing date 2023-09-29
    Publishing country England
    Document type Editorial ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1093/cvr/cvad156
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  7. Article ; Online: Why animal model studies are lost in translation.

    Frangogiannis, Nikolaos G

    The journal of cardiovascular aging

    2022  Volume 2, Issue 2

    Abstract: The development of novel therapies based on understanding the pathophysiologic basis of disease is a major goal of biomedical research. Despite an explosion in new knowledge on the molecular mechanisms of disease derived from animal model investigations, ...

    Abstract The development of novel therapies based on understanding the pathophysiologic basis of disease is a major goal of biomedical research. Despite an explosion in new knowledge on the molecular mechanisms of disease derived from animal model investigations, translation into effective treatment for human patients has been disappointingly slow. Several fundamental problems may explain the translational failures. First, the emphasis on novel and highly significant findings selectively rewards implausible, low-probability observations and high-magnitude effects, providing a biased perspective of the pathophysiology of disease that underappreciates the complexity and redundancy of biological systems. Second, even when a sound targetable mechanism is identified, animal models cannot recapitulate the pathophysiologic heterogeneity of the human disease, and are poor predictors of therapeutic success. Third, traditional classifications of most complex diseases are based primarily on clinical criteria and do not reflect the diverse pathophysiologic mechanisms that may be involved. The development of a flexible and dynamic conceptual paradigm that takes into account the totality of the evidence on the mechanisms of disease, and pathophysiologic stratification of patients to identify subpopulations with distinct pathogenetic mechanisms, are crucial for the development of new therapeutics.
    Language English
    Publishing date 2022-03-31
    Publishing country United States
    Document type Journal Article
    ISSN 2768-5993
    ISSN (online) 2768-5993
    DOI 10.20517/jca.2022.10
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  8. Article ; Online: Transforming growth factor-β in myocardial disease.

    Frangogiannis, Nikolaos G

    Nature reviews. Cardiology

    2022  Volume 19, Issue 7, Page(s) 435–455

    Abstract: Transforming growth factor-β (TGFβ) isoforms are upregulated and activated in myocardial diseases and have an important role in cardiac repair and remodelling, regulating the phenotype and function of cardiomyocytes, fibroblasts, immune cells and ... ...

    Abstract Transforming growth factor-β (TGFβ) isoforms are upregulated and activated in myocardial diseases and have an important role in cardiac repair and remodelling, regulating the phenotype and function of cardiomyocytes, fibroblasts, immune cells and vascular cells. Cardiac injury triggers the generation of bioactive TGFβ from latent stores, through mechanisms involving proteases, integrins and specialized extracellular matrix (ECM) proteins. Activated TGFβ signals through the SMAD intracellular effectors or through non-SMAD cascades. In the infarcted heart, the anti-inflammatory and fibroblast-activating actions of TGFβ have an important role in repair; however, excessive or prolonged TGFβ signalling accentuates adverse remodelling, contributing to cardiac dysfunction. Cardiac pressure overload also activates TGFβ cascades, which initially can have a protective role, promoting an ECM-preserving phenotype in fibroblasts and preventing the generation of injurious, pro-inflammatory ECM fragments. However, prolonged and overactive TGFβ signalling in pressure-overloaded cardiomyocytes and fibroblasts can promote cardiac fibrosis and dysfunction. In the atria, TGFβ-mediated fibrosis can contribute to the pathogenic substrate for atrial fibrillation. Overactive or dysregulated TGFβ responses have also been implicated in cardiac ageing and in the pathogenesis of diabetic, genetic and inflammatory cardiomyopathies. This Review summarizes the current evidence on the role of TGFβ signalling in myocardial diseases, focusing on cellular targets and molecular mechanisms, and discussing challenges and opportunities for therapeutic translation.
    MeSH term(s) Cardiomyopathies/metabolism ; Extracellular Matrix Proteins/genetics ; Extracellular Matrix Proteins/metabolism ; Fibroblasts/metabolism ; Fibrosis ; Humans ; Myocytes, Cardiac/metabolism ; Transforming Growth Factor beta/genetics ; Transforming Growth Factor beta/metabolism ; Transforming Growth Factors/metabolism
    Chemical Substances Extracellular Matrix Proteins ; Transforming Growth Factor beta ; Transforming Growth Factors (76057-06-2)
    Language English
    Publishing date 2022-01-04
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 2490375-9
    ISSN 1759-5010 ; 1759-5002
    ISSN (online) 1759-5010
    ISSN 1759-5002
    DOI 10.1038/s41569-021-00646-w
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  9. Article ; Online: Platelet-derived growth factor (PDGF) therapy in myocardial infarction: Challenges and opportunities.

    Frangogiannis, Nikolaos G

    International journal of cardiology

    2021  Volume 341, Page(s) 74–75

    MeSH term(s) Humans ; Myocardial Infarction/diagnosis ; Myocardial Infarction/drug therapy ; Platelet-Derived Growth Factor
    Chemical Substances Platelet-Derived Growth Factor
    Language English
    Publishing date 2021-08-18
    Publishing country Netherlands
    Document type Editorial ; Comment
    ZDB-ID 779519-1
    ISSN 1874-1754 ; 0167-5273
    ISSN (online) 1874-1754
    ISSN 0167-5273
    DOI 10.1016/j.ijcard.2021.08.022
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  10. Article ; Online: Fact and Fiction About Fibroblast to Endothelium Conversion: Semantics and Substance of Cellular Identity.

    Frangogiannis, Nikolaos G

    Circulation

    2020  Volume 142, Issue 17, Page(s) 1663–1666

    MeSH term(s) Endothelium ; Fibroblasts ; Humans ; Semantics
    Language English
    Publishing date 2020-10-26
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.120.050875
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