Endothelial-to-mesenchymal transition: Cytokine-mediated pathways that determine endothelial fibrosis under inflammatory conditions

Lorena Pérez, Natalia Muñoz-Durango, Claudia A. Riedel, Cesar Echeverría, Alexis M. Kalergis, Claudio Cabello-Verrugio, Felipe Simon

Resultado de la investigación: Research - revisión exhaustivaShort survey

  • 5 Citas

Resumen

During the last decade, the endothelial-to-mesenchymal transition (EndMT) process has attracted considerable attention due to associations with the onset of certain diseases, such as organ fibrosis and cancer. Several studies have assessed the mechanisms and signaling pathways that regulate endothelial fibrosis in the context of human pathologies. A number of inflammatory mediators, including pro-inflammatory cytokines, growth factors, oxidative stress, and toxins, induce the conversion of endothelial cells into mesenchymal fibroblast-like cells that promote disease progression. This review is separated into five chapters that critically present current knowledge on EndMT in the context of pathology. First, the main characteristics of EndMT are summarized, with a focus on the endothelial protein pattern changes that modulate the expressions of endothelial/fibrotic markers and extracellular matrix proteins. These expressions could serve as mechanisms for explaining potential EndMT contributions to human pathologies in adults. Second, the main findings supporting a connection between EndMT-mediated endothelial fibrosis and inflammatory conditions are presented. These connections could be linked to the onset and progression of pathological conditions. Third, EndMT inducers are described in detail. This includes considerations on the actions of the first and most well-known EndMT inducer, TGF-β; of the most prominent pro-inflammatory cytokines released during inflammation, such as IL 1-β and TNF-α; and of the NF-κB transcription factor, a common player during inflammation-induced EndMT. Furthermore, thorough attention is given to EndMT induction by endotoxins in the context of bacterial infectious diseases. Additionally, the participation of the inflammatory oxidative stress environment in the EndMT induction was also reviewed. Fourth, the pathophysiological findings of inflammation-induced EndMT are presented, and, fifth, special focus is placed on associations with cancer onset and development. Altogether, this review highlights the important role of EndMT-mediated endothelial fibrosis during inflammation in human pathologies.

IdiomaEnglish
Páginas41-54
Número de páginas14
PublicaciónCytokine and Growth Factor Reviews
Volumen33
DOI
EstadoPublished - 1 feb 2017

Huella dactilar

Fibrosis
Pathology
Cytokines
Inflammation
Oxidative Stress
Neoplasms
Oxidative stress
Extracellular Matrix Proteins
Interleukin-1beta
Endotoxins
Transforming Growth Factor beta
Communicable Diseases
Disease Progression
Intercellular Signaling Peptides and Proteins
Transcription Factors
Endothelial Cells
Tumor Necrosis Factor-alpha
Fibroblasts
Proteins
Endothelial cells

Keywords

    ASJC Scopus subject areas

    • Immunology and Allergy
    • Endocrinology, Diabetes and Metabolism
    • Immunology
    • Biochemistry, Genetics and Molecular Biology(all)

    Citar esto

    @article{3105eaeb3470406a8e51f38a79dfdc3a,
    title = "Endothelial-to-mesenchymal transition: Cytokine-mediated pathways that determine endothelial fibrosis under inflammatory conditions",
    abstract = "During the last decade, the endothelial-to-mesenchymal transition (EndMT) process has attracted considerable attention due to associations with the onset of certain diseases, such as organ fibrosis and cancer. Several studies have assessed the mechanisms and signaling pathways that regulate endothelial fibrosis in the context of human pathologies. A number of inflammatory mediators, including pro-inflammatory cytokines, growth factors, oxidative stress, and toxins, induce the conversion of endothelial cells into mesenchymal fibroblast-like cells that promote disease progression. This review is separated into five chapters that critically present current knowledge on EndMT in the context of pathology. First, the main characteristics of EndMT are summarized, with a focus on the endothelial protein pattern changes that modulate the expressions of endothelial/fibrotic markers and extracellular matrix proteins. These expressions could serve as mechanisms for explaining potential EndMT contributions to human pathologies in adults. Second, the main findings supporting a connection between EndMT-mediated endothelial fibrosis and inflammatory conditions are presented. These connections could be linked to the onset and progression of pathological conditions. Third, EndMT inducers are described in detail. This includes considerations on the actions of the first and most well-known EndMT inducer, TGF-β; of the most prominent pro-inflammatory cytokines released during inflammation, such as IL 1-β and TNF-α; and of the NF-κB transcription factor, a common player during inflammation-induced EndMT. Furthermore, thorough attention is given to EndMT induction by endotoxins in the context of bacterial infectious diseases. Additionally, the participation of the inflammatory oxidative stress environment in the EndMT induction was also reviewed. Fourth, the pathophysiological findings of inflammation-induced EndMT are presented, and, fifth, special focus is placed on associations with cancer onset and development. Altogether, this review highlights the important role of EndMT-mediated endothelial fibrosis during inflammation in human pathologies.",
    keywords = "Endothelium, Fibrosis, Inflammation, Interleukin, TGF-β, TNF-α",
    author = "Lorena Pérez and Natalia Muñoz-Durango and Riedel, {Claudia A.} and Cesar Echeverría and Kalergis, {Alexis M.} and Claudio Cabello-Verrugio and Felipe Simon",
    year = "2017",
    month = "2",
    doi = "10.1016/j.cytogfr.2016.09.002",
    volume = "33",
    pages = "41--54",
    journal = "Cytokine and Growth Factor Reviews",
    issn = "1359-6101",
    publisher = "Elsevier BV",

    }

    Endothelial-to-mesenchymal transition : Cytokine-mediated pathways that determine endothelial fibrosis under inflammatory conditions. / Pérez, Lorena; Muñoz-Durango, Natalia; Riedel, Claudia A.; Echeverría, Cesar; Kalergis, Alexis M.; Cabello-Verrugio, Claudio; Simon, Felipe.

    En: Cytokine and Growth Factor Reviews, Vol. 33, 01.02.2017, p. 41-54.

    Resultado de la investigación: Research - revisión exhaustivaShort survey

    TY - JOUR

    T1 - Endothelial-to-mesenchymal transition

    T2 - Cytokine and Growth Factor Reviews

    AU - Pérez,Lorena

    AU - Muñoz-Durango,Natalia

    AU - Riedel,Claudia A.

    AU - Echeverría,Cesar

    AU - Kalergis,Alexis M.

    AU - Cabello-Verrugio,Claudio

    AU - Simon,Felipe

    PY - 2017/2/1

    Y1 - 2017/2/1

    N2 - During the last decade, the endothelial-to-mesenchymal transition (EndMT) process has attracted considerable attention due to associations with the onset of certain diseases, such as organ fibrosis and cancer. Several studies have assessed the mechanisms and signaling pathways that regulate endothelial fibrosis in the context of human pathologies. A number of inflammatory mediators, including pro-inflammatory cytokines, growth factors, oxidative stress, and toxins, induce the conversion of endothelial cells into mesenchymal fibroblast-like cells that promote disease progression. This review is separated into five chapters that critically present current knowledge on EndMT in the context of pathology. First, the main characteristics of EndMT are summarized, with a focus on the endothelial protein pattern changes that modulate the expressions of endothelial/fibrotic markers and extracellular matrix proteins. These expressions could serve as mechanisms for explaining potential EndMT contributions to human pathologies in adults. Second, the main findings supporting a connection between EndMT-mediated endothelial fibrosis and inflammatory conditions are presented. These connections could be linked to the onset and progression of pathological conditions. Third, EndMT inducers are described in detail. This includes considerations on the actions of the first and most well-known EndMT inducer, TGF-β; of the most prominent pro-inflammatory cytokines released during inflammation, such as IL 1-β and TNF-α; and of the NF-κB transcription factor, a common player during inflammation-induced EndMT. Furthermore, thorough attention is given to EndMT induction by endotoxins in the context of bacterial infectious diseases. Additionally, the participation of the inflammatory oxidative stress environment in the EndMT induction was also reviewed. Fourth, the pathophysiological findings of inflammation-induced EndMT are presented, and, fifth, special focus is placed on associations with cancer onset and development. Altogether, this review highlights the important role of EndMT-mediated endothelial fibrosis during inflammation in human pathologies.

    AB - During the last decade, the endothelial-to-mesenchymal transition (EndMT) process has attracted considerable attention due to associations with the onset of certain diseases, such as organ fibrosis and cancer. Several studies have assessed the mechanisms and signaling pathways that regulate endothelial fibrosis in the context of human pathologies. A number of inflammatory mediators, including pro-inflammatory cytokines, growth factors, oxidative stress, and toxins, induce the conversion of endothelial cells into mesenchymal fibroblast-like cells that promote disease progression. This review is separated into five chapters that critically present current knowledge on EndMT in the context of pathology. First, the main characteristics of EndMT are summarized, with a focus on the endothelial protein pattern changes that modulate the expressions of endothelial/fibrotic markers and extracellular matrix proteins. These expressions could serve as mechanisms for explaining potential EndMT contributions to human pathologies in adults. Second, the main findings supporting a connection between EndMT-mediated endothelial fibrosis and inflammatory conditions are presented. These connections could be linked to the onset and progression of pathological conditions. Third, EndMT inducers are described in detail. This includes considerations on the actions of the first and most well-known EndMT inducer, TGF-β; of the most prominent pro-inflammatory cytokines released during inflammation, such as IL 1-β and TNF-α; and of the NF-κB transcription factor, a common player during inflammation-induced EndMT. Furthermore, thorough attention is given to EndMT induction by endotoxins in the context of bacterial infectious diseases. Additionally, the participation of the inflammatory oxidative stress environment in the EndMT induction was also reviewed. Fourth, the pathophysiological findings of inflammation-induced EndMT are presented, and, fifth, special focus is placed on associations with cancer onset and development. Altogether, this review highlights the important role of EndMT-mediated endothelial fibrosis during inflammation in human pathologies.

    KW - Endothelium

    KW - Fibrosis

    KW - Inflammation

    KW - Interleukin

    KW - TGF-β

    KW - TNF-α

    UR - http://www.scopus.com/inward/record.url?scp=84998980152&partnerID=8YFLogxK

    U2 - 10.1016/j.cytogfr.2016.09.002

    DO - 10.1016/j.cytogfr.2016.09.002

    M3 - Short survey

    VL - 33

    SP - 41

    EP - 54

    JO - Cytokine and Growth Factor Reviews

    JF - Cytokine and Growth Factor Reviews

    SN - 1359-6101

    ER -