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  1. Article: Modeling the microenvironment special issue.

    Leask, Andrew

    Journal of cell communication and signaling

    2022  Volume 16, Issue 4, Page(s) 631–632

    Language English
    Publishing date 2022-03-29
    Publishing country Netherlands
    Document type Editorial
    ZDB-ID 2299380-0
    ISSN 1873-961X ; 1873-9601
    ISSN (online) 1873-961X
    ISSN 1873-9601
    DOI 10.1007/s12079-022-00675-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Yay team!: 5.782.

    Leask, Andrew

    Journal of cell communication and signaling

    2021  Volume 15, Issue 4, Page(s) 473

    Language English
    Publishing date 2021-07-22
    Publishing country Netherlands
    Document type Editorial
    ZDB-ID 2299380-0
    ISSN 1873-961X ; 1873-9601
    ISSN (online) 1873-961X
    ISSN 1873-9601
    DOI 10.1007/s12079-021-00636-0
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  3. Article: Welcome to 2021.

    Leask, Andrew

    Journal of cell communication and signaling

    2021  Volume 15, Issue 1, Page(s) 5

    Language English
    Publishing date 2021-01-25
    Publishing country Netherlands
    Document type Editorial
    ZDB-ID 2299380-0
    ISSN 1873-961X ; 1873-9601
    ISSN (online) 1873-961X
    ISSN 1873-9601
    DOI 10.1007/s12079-021-00606-6
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  4. Article ; Online: The role of positional information in determining dermal fibroblast diversity.

    Chitturi, Pratyusha / Leask, Andrew

    Matrix biology : journal of the International Society for Matrix Biology

    2024  Volume 128, Page(s) 31–38

    Abstract: The largest mammalian organ, skin, consisting of a dermal connective tissue layer that underlies and supports the epidermis, acts as a protective barrier that excludes external pathogens and disseminates sensory signals emanating from the local ... ...

    Abstract The largest mammalian organ, skin, consisting of a dermal connective tissue layer that underlies and supports the epidermis, acts as a protective barrier that excludes external pathogens and disseminates sensory signals emanating from the local microenvironment. Dermal connective tissue is comprised of a collagen-rich extracellular matrix (ECM) that is produced by connective tissue fibroblasts resident within the dermis. When wounded, a tissue repair program is induced whereby fibroblasts, in response to alterations in the microenvironment, produce new ECM components, resulting in the formation of a scar. Failure to terminate the normal tissue repair program causes fibrotic conditions including: hypertrophic scars, keloids, and the systemic autoimmune connective tissue disease scleroderma (systemic sclerosis, SSc). Histological and single-cell RNA sequencing (scRNAseq) studies have revealed that fibroblasts are heterogeneous and highly plastic. Understanding how this diversity contributes to dermal homeostasis, wounding, fibrosis, and cancer may ultimately result in novel anti-fibrotic therapies and personalized medicine. This review summarizes studies supporting this concept.
    MeSH term(s) Animals ; Cicatrix, Hypertrophic ; Epidermis/pathology ; Fibroblasts/pathology ; Fibrosis ; Mammals ; Scleroderma, Systemic/genetics ; Scleroderma, Systemic/pathology ; Skin/pathology
    Language English
    Publishing date 2024-02-28
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 1183793-7
    ISSN 1569-1802 ; 0945-053X
    ISSN (online) 1569-1802
    ISSN 0945-053X
    DOI 10.1016/j.matbio.2024.02.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1694: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article: Blisters on your fingers.

    Leask, Andrew

    Journal of cell communication and signaling

    2021  Volume 15, Issue 3, Page(s) 465–466

    Abstract: Mesenchymal progenitor cells play a key role in fibrogenesis. An exciting paper was recently published showed that blister fluid from the skin patients with the autoimmune connective tissue disease scleroderma (systemic sclerosis, SSc) preferentially ... ...

    Abstract Mesenchymal progenitor cells play a key role in fibrogenesis. An exciting paper was recently published showed that blister fluid from the skin patients with the autoimmune connective tissue disease scleroderma (systemic sclerosis, SSc) preferentially activated mesenchymal progenitor cells (Taki et al. in Arthritis Rheumatol 72(8):1361-1374, 2020). These data provide new and invaluable insights into the complex interactions in the connective tissue microenvironment that ultimately result in persistent, pathological fibrosis.
    Language English
    Publishing date 2021-05-20
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2299380-0
    ISSN 1873-961X ; 1873-9601
    ISSN (online) 1873-961X
    ISSN 1873-9601
    DOI 10.1007/s12079-021-00626-2
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  6. Article ; Online: The hard problem: Mechanotransduction perpetuates the myofibroblast phenotype in scleroderma fibrosis.

    Leask, Andrew

    Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society

    2021  Volume 29, Issue 4, Page(s) 582–587

    Abstract: The effector cells ultimately responsible for fibrosis are myofibroblasts. In the fibrotic autoimmune connective tissue disease scleroderma, myofibroblasts are autonomously activated, and retain their phenotype upon culturing. Since the 1990s, ... ...

    Abstract The effector cells ultimately responsible for fibrosis are myofibroblasts. In the fibrotic autoimmune connective tissue disease scleroderma, myofibroblasts are autonomously activated, and retain their phenotype upon culturing. Since the 1990s, researchers have exploited this fact to use scleroderma fibroblasts as a model system to uncover the fundamental mechanisms underlying myofibroblast persistence in fibrotic conditions. These studies have suggested that an autocrine transforming growth factor (TGF)beta signaling loop is insufficient to explain the persistent myofibroblast phenotype but instead support the hypothesis that fibrotic myofibroblasts possess an intrinsically activated pro-adhesive signaling pathway, and that this contributes to the perpetuation of pathological fibrosis. This review focuses on these observations.
    MeSH term(s) Cell Differentiation ; Fibroblasts ; Fibrosis ; Humans ; Mechanotransduction, Cellular ; Myofibroblasts/pathology ; Phenotype ; Transforming Growth Factor beta ; Transforming Growth Factor beta1 ; Wound Healing
    Chemical Substances Transforming Growth Factor beta ; Transforming Growth Factor beta1
    Language English
    Publishing date 2021-01-07
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1174873-4
    ISSN 1524-475X ; 1067-1927
    ISSN (online) 1524-475X
    ISSN 1067-1927
    DOI 10.1111/wrr.12889
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3890: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  7. Article: What a long, strange trip it's been.

    Leask, Andrew

    Journal of cell communication and signaling

    2020  Volume 14, Issue 1, Page(s) 19–20

    Language English
    Publishing date 2020-03-13
    Publishing country Netherlands
    Document type Editorial
    ZDB-ID 2299380-0
    ISSN 1873-961X ; 1873-9601
    ISSN (online) 1873-961X
    ISSN 1873-9601
    DOI 10.1007/s12079-020-00555-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: COVID-19: is fibrosis the killer?

    Leask, Andrew

    Journal of cell communication and signaling

    2020  Volume 14, Issue 2, Page(s) 255

    Abstract: COVID-19 is a respiratory disease. A recent report in Lancet examined, retrospectively, 137 patients with COVD-19. Patients that died had elevated IL-6 levels and acute respiratory distress syndrome. These data have obvious implications for how to ... ...

    Abstract COVID-19 is a respiratory disease. A recent report in Lancet examined, retrospectively, 137 patients with COVD-19. Patients that died had elevated IL-6 levels and acute respiratory distress syndrome. These data have obvious implications for how to control mortality in COVID-19.
    Keywords covid19
    Language English
    Publishing date 2020-05-01
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2299380-0
    ISSN 1873-961X ; 1873-9601
    ISSN (online) 1873-961X
    ISSN 1873-9601
    DOI 10.1007/s12079-020-00569-0
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  9. Article: Et tu, CCN1….

    Leask, Andrew

    Journal of cell communication and signaling

    2020  Volume 14, Issue 3, Page(s) 355–356

    Abstract: The CCN family of matricellular proteins are recognized bona fide targets for therapeutically targeting so-called chronic inflammatory diseases, including fibrosis and cancers. The majority of the work supporting this contention has been derived from ... ...

    Abstract The CCN family of matricellular proteins are recognized bona fide targets for therapeutically targeting so-called chronic inflammatory diseases, including fibrosis and cancers. The majority of the work supporting this contention has been derived from examining CCN2, formerly, and unhelpfully, termed "connective tissue growth factor." Both CCN2, and its related protein, CCN1, formerly termed "cysteine-rich protein 61", are positively regulated by not only TGFbeta, but also by the hippo/YAP/TAZ mechanotransduction pathway that appears to drive these pathologies. Indeed, increasing evidence indicates that CCN1 also contributes to these fibrosis and cancers and, consequently, targeting both CCN2 and CCN1 simultaneously could be of therapeutic value. This commentary focuses on a recent, exciting paper (Ju et al., 2020, Scientific Reports, 10, 3201) suggesting that CCN1 is a target for non-alcoholic steatohepatitis (NASH).
    Language English
    Publishing date 2020-07-23
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2299380-0
    ISSN 1873-961X ; 1873-9601
    ISSN (online) 1873-961X
    ISSN 1873-9601
    DOI 10.1007/s12079-020-00573-4
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  10. Article: Slow train coming: an anti-CCN2 strategy reverses a model of chronic overuse muscle fibrosis.

    Leask, Andrew

    Journal of cell communication and signaling

    2020  Volume 14, Issue 3, Page(s) 349–350

    Abstract: One of the first targets proposed as an anti-fibrotic therapy was CCN2. Proof of its involvement in fibrosis was initially difficult, due to the lack of appropriate reagents and general understanding of the molecular mechanisms responsible for persistent ...

    Abstract One of the first targets proposed as an anti-fibrotic therapy was CCN2. Proof of its involvement in fibrosis was initially difficult, due to the lack of appropriate reagents and general understanding of the molecular mechanisms responsible for persistent fibrosis. As these issues have been progressively resolved over the last twenty-five years, it has become clear that CCN2 is a bone fide target for anti-fibrotic intervention. An anti-CCN2 antibody (FG-3019) is in Phase III clinical trials for idiopathic pulmonary fibrosis and pancreatic cancer, and in Phase II for Duschenne's muscular dystrophy. An exciting paper recently published by Mary Barbe and the Popoff group has shown that FG-3019 reduces established muscle fibrosis (Barbe et al., FASEB J 34:6554-6569, 2020). Intriguingly, FG-3019 blocked the decreased expression of the anti-fibrotic protein CCN3, caused by the injury model. These important data support the notion that targeting CCN2 in the fibrotic microenvironment may reverse established fibrosis, making it the first agent currently in development to do so.
    Language English
    Publishing date 2020-05-14
    Publishing country Netherlands
    Document type Editorial
    ZDB-ID 2299380-0
    ISSN 1873-961X ; 1873-9601
    ISSN (online) 1873-961X
    ISSN 1873-9601
    DOI 10.1007/s12079-020-00568-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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