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  1. Article ; Online: Pulmonary fibrosis: Emerging diagnostic and therapeutic strategies.

    Selvarajah, Brintha / Platé, Manuela / Chambers, Rachel C

    Molecular aspects of medicine

    2023  Volume 94, Page(s) 101227

    Abstract: Fibrosis is the concluding pathological outcome and major cause of morbidity and mortality in a number of common chronic inflammatory, immune-mediated and metabolic diseases. The progressive deposition of a collagen-rich extracellular matrix (ECM) ... ...

    Abstract Fibrosis is the concluding pathological outcome and major cause of morbidity and mortality in a number of common chronic inflammatory, immune-mediated and metabolic diseases. The progressive deposition of a collagen-rich extracellular matrix (ECM) represents the cornerstone of the fibrotic response and culminates in organ failure and premature death. Idiopathic pulmonary fibrosis (IPF) represents the most rapidly progressive and lethal of all fibrotic diseases with a dismal median survival of 3.5 years from diagnosis. Although the approval of the antifibrotic agents, pirfenidone and nintedanib, for the treatment of IPF signalled a watershed moment for the development of anti-fibrotic therapeutics, these agents slow but do not halt disease progression or improve quality of life. There therefore remains a pressing need for the development of effective therapeutic strategies. In this article, we review emerging therapeutic strategies for IPF as well as the pre-clinical and translational approaches that will underpin a greater understanding of the key pathomechanisms involved in order to transform the way we diagnose and treat pulmonary fibrosis.
    MeSH term(s) Humans ; Quality of Life ; Idiopathic Pulmonary Fibrosis/diagnosis ; Idiopathic Pulmonary Fibrosis/drug therapy ; Fibrosis ; Inflammation/metabolism ; Extracellular Matrix/metabolism
    Language English
    Publishing date 2023-11-24
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 197640-0
    ISSN 1872-9452 ; 0098-2997
    ISSN (online) 1872-9452
    ISSN 0098-2997
    DOI 10.1016/j.mam.2023.101227
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Fibrometabolism-An emerging therapeutic frontier in pulmonary fibrosis.

    Selvarajah, Brintha / Azuelos, Ilan / Anastasiou, Dimitrios / Chambers, Rachel C

    Science signaling

    2021  Volume 14, Issue 697

    Abstract: Fibrosis is the final pathological outcome and major cause of morbidity and mortality in many common and chronic inflammatory, immune-mediated, and metabolic diseases. Despite the growing incidence of fibrotic diseases and extensive research efforts, ... ...

    Abstract Fibrosis is the final pathological outcome and major cause of morbidity and mortality in many common and chronic inflammatory, immune-mediated, and metabolic diseases. Despite the growing incidence of fibrotic diseases and extensive research efforts, there remains a lack of effective therapies that improve survival. The application of omics technologies has revolutionized our approach to identifying previously unknown therapeutic targets and potential disease biomarkers. The application of metabolomics, in particular, has improved our understanding of disease pathomechanisms and garnered a wave of scientific interest in the role of metabolism in the biology of myofibroblasts, the key effector cells of the fibrogenic response. Emerging evidence suggests that alterations in metabolism not only are a feature of but also may play an influential role in the pathogenesis of fibrosis, most notably in idiopathic pulmonary fibrosis (IPF), the most rapidly progressive and fatal of all fibrotic conditions. This review will detail the role of key metabolic pathways, their alterations in myofibroblasts, and the potential this new knowledge offers for the development of antifibrotic therapeutic strategies.
    MeSH term(s) Fibrosis ; Humans ; Idiopathic Pulmonary Fibrosis/pathology ; Idiopathic Pulmonary Fibrosis/therapy ; Myofibroblasts/pathology
    Language English
    Publishing date 2021-08-24
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2417226-1
    ISSN 1937-9145 ; 1945-0877
    ISSN (online) 1937-9145
    ISSN 1945-0877
    DOI 10.1126/scisignal.aay1027
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: mTORC1 amplifies the ATF4-dependent de novo serine-glycine pathway to supply glycine during TGF-β

    Selvarajah, Brintha / Azuelos, Ilan / Platé, Manuela / Guillotin, Delphine / Forty, Ellen J / Contento, Greg / Woodcock, Hannah V / Redding, Matthew / Taylor, Adam / Brunori, Gino / Durrenberger, Pascal F / Ronzoni, Riccardo / Blanchard, Andy D / Mercer, Paul F / Anastasiou, Dimitrios / Chambers, Rachel C

    Science signaling

    2019  Volume 12, Issue 582

    Abstract: The differentiation of fibroblasts into a transient population of highly activated, extracellular matrix (ECM)-producing myofibroblasts at sites of tissue injury is critical for normal tissue repair. Excessive myofibroblast accumulation and persistence, ... ...

    Abstract The differentiation of fibroblasts into a transient population of highly activated, extracellular matrix (ECM)-producing myofibroblasts at sites of tissue injury is critical for normal tissue repair. Excessive myofibroblast accumulation and persistence, often as a result of a failure to undergo apoptosis when tissue repair is complete, lead to pathological fibrosis and are also features of the stromal response in cancer. Myofibroblast differentiation is accompanied by changes in cellular metabolism, including increased glycolysis, to meet the biosynthetic demands of enhanced ECM production. Here, we showed that transforming growth factor-β
    MeSH term(s) Activating Transcription Factor 4/genetics ; Activating Transcription Factor 4/metabolism ; Biosynthetic Pathways/drug effects ; Biosynthetic Pathways/genetics ; Cell Differentiation/drug effects ; Cell Differentiation/genetics ; Cells, Cultured ; Collagen/biosynthesis ; Extracellular Matrix/metabolism ; Fibroblasts/cytology ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Gene Expression Regulation/drug effects ; Glycine/biosynthesis ; Humans ; Mechanistic Target of Rapamycin Complex 1/genetics ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Myofibroblasts/cytology ; Myofibroblasts/drug effects ; Myofibroblasts/metabolism ; Serine/biosynthesis ; Signal Transduction/drug effects ; Transforming Growth Factor beta1/pharmacology
    Chemical Substances Transforming Growth Factor beta1 ; Activating Transcription Factor 4 (145891-90-3) ; Serine (452VLY9402) ; Collagen (9007-34-5) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Glycine (TE7660XO1C)
    Language English
    Publishing date 2019-05-21
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2417226-1
    ISSN 1937-9145 ; 1945-0877
    ISSN (online) 1937-9145
    ISSN 1945-0877
    DOI 10.1126/scisignal.aav3048
    Database MEDical Literature Analysis and Retrieval System OnLINE

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