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Title:
TGF-β in fibrosis by acting as a conductor for contractile properties of myofibroblasts | Cell & Bioscience
Description:
Myofibroblasts are non-muscle contractile cells that play a key physiologically role in organs such as the stem villi of the human placenta during physiological pregnancy. They are able to contract and relax in response to changes in the volume of the intervillous chamber. Myofibroblasts have also been observed in several diseases and are involved in wound healing and the fibrotic processes affecting several organs, such as the liver, lungs, kidneys and heart. During the fibrotic process, tissue retraction rather than contraction is correlated with collagen synthesis in the extracellular matrix, leading to irreversible fibrosis and, finally, apoptosis of myofibroblasts. The molecular motor of myofibroblasts is the non-muscle type IIA and B myosin (NMMIIA and NMMIIB). Fibroblast differentiation into myofibroblasts is largely governed by the transforming growth factor-β1 (TGF-β1). This system controls the canonical WNT/β-catenin pathway in a positive manner, and PPARγ in a negative manner. The WNT/β-catenin pathway promotes fibrosis, while PPARγ prevents it. This review focuses on the contractile properties of myofibroblasts and the conductor, TGF-β1, which together control the opposing interplay between PPARγ and the canonical WNT/β-catenin pathway.
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Keywords {🔍}
pubmed, article, google, scholar, cas, pparγ, tgfβ, fibrosis, myofibroblasts, cells, central, signaling, pathway, canonical, wnt, cell, differentiation, human, smad, contractile, tissue, activation, role, vallée, myofibroblast, fibroblasts, fibrotic, wntβcatenin, expression, growth, peroxisome, receptor, biol, proliferatoractivated, observed, process, muscle, lecarpentier, wound, kinase, physiol, stem, ligands, myosin, factor, complex, gamma, taz, collagen, protein,
Topics {✒️}
peroxisome proliferator-activated receptor-alpha peroxisome proliferator-activated receptor-gamma peroxisome proliferator-activated receptor-γ tgf-β1-induced sapk/jnk signaling tgf-beta1-induced epithelial-mesenchymal transition tgf-β1/wnt/β-catenin pathway camkii-tak1-nlk-tab 2 inhibits canonical wnt/beta-catenin pathway peroxisome proliferator-activated receptor l-amino acid-defined diet canonical wnt/β-catenin pathway canonical wnt/-β-catenin pathway canonical wnt/β-catenin signaling transforming growth factor-beta transforming growth factor-beta1 prevent tgf-β1-induced fibrosis serine/threonine protein kinase transforming growth factor-β1 glycogen synthase kinase-3β peroxisome proliferator-activated receptors tgf-beta1-induced myofibroblast differentiation prevent β-catenin degradation tgf-β-induced pi3k/akt atp-adp-pi actin-myosin interaction beta-catenin/lef-1 pathway platelet-derived growth factor nf-e2-related factor 2 canonical wnt/β-catenin il-6 nf-kappab induced low-density lipoprotein receptor wnt/β-catenin pathway smad-independent tgf-β1 signaling article download pdf myocyte β1-adrenergic receptor wnt/β-catenin signaling wnt/beta-catenin pathways alpha-smooth muscle actin g-protein coupled receptor tgf-β induced collagen pparγ-induced tensin homologue β-catenin destruction complex bleomycin-induced pulmonary fibrosis gsk-3β activity leads cadherin-mediated cell adhesion β-catenin-dependent manner collagen-induced profibrotic signal tgf-β1 tgf-β αvβ6 stimulate tgf-β1 β-catenin target genes tgf-β-mediated fibrosis
Questions {❓}
- Canonical Wnt signalling as a key regulator of fibrogenesis—implications for targeted therapies?
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mainEntity:
headline:TGF-β in fibrosis by acting as a conductor for contractile properties of myofibroblasts
description:Myofibroblasts are non-muscle contractile cells that play a key physiologically role in organs such as the stem villi of the human placenta during physiological pregnancy. They are able to contract and relax in response to changes in the volume of the intervillous chamber. Myofibroblasts have also been observed in several diseases and are involved in wound healing and the fibrotic processes affecting several organs, such as the liver, lungs, kidneys and heart. During the fibrotic process, tissue retraction rather than contraction is correlated with collagen synthesis in the extracellular matrix, leading to irreversible fibrosis and, finally, apoptosis of myofibroblasts. The molecular motor of myofibroblasts is the non-muscle type IIA and B myosin (NMMIIA and NMMIIB). Fibroblast differentiation into myofibroblasts is largely governed by the transforming growth factor-β1 (TGF-β1). This system controls the canonical WNT/β-catenin pathway in a positive manner, and PPARγ in a negative manner. The WNT/β-catenin pathway promotes fibrosis, while PPARγ prevents it. This review focuses on the contractile properties of myofibroblasts and the conductor, TGF-β1, which together control the opposing interplay between PPARγ and the canonical WNT/β-catenin pathway.
datePublished:2019-12-09T00:00:00Z
dateModified:2019-12-09T00:00:00Z
pageStart:1
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license:http://creativecommons.org/licenses/by/4.0/
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keywords:
Transforming growth factor-β1
PPARγ
Canonical WNT/-β-catenin
YAP/TAZ
Smad
Myofibroblasts
Fibrosis
Myosin
Cell Biology
Microbiology
Stem Cells
Neurobiology
Proteomics
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headline:TGF-β in fibrosis by acting as a conductor for contractile properties of myofibroblasts
description:Myofibroblasts are non-muscle contractile cells that play a key physiologically role in organs such as the stem villi of the human placenta during physiological pregnancy. They are able to contract and relax in response to changes in the volume of the intervillous chamber. Myofibroblasts have also been observed in several diseases and are involved in wound healing and the fibrotic processes affecting several organs, such as the liver, lungs, kidneys and heart. During the fibrotic process, tissue retraction rather than contraction is correlated with collagen synthesis in the extracellular matrix, leading to irreversible fibrosis and, finally, apoptosis of myofibroblasts. The molecular motor of myofibroblasts is the non-muscle type IIA and B myosin (NMMIIA and NMMIIB). Fibroblast differentiation into myofibroblasts is largely governed by the transforming growth factor-β1 (TGF-β1). This system controls the canonical WNT/β-catenin pathway in a positive manner, and PPARγ in a negative manner. The WNT/β-catenin pathway promotes fibrosis, while PPARγ prevents it. This review focuses on the contractile properties of myofibroblasts and the conductor, TGF-β1, which together control the opposing interplay between PPARγ and the canonical WNT/β-catenin pathway.
datePublished:2019-12-09T00:00:00Z
dateModified:2019-12-09T00:00:00Z
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license:http://creativecommons.org/licenses/by/4.0/
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keywords:
Transforming growth factor-β1
PPARγ
Canonical WNT/-β-catenin
YAP/TAZ
Smad
Myofibroblasts
Fibrosis
Myosin
Cell Biology
Microbiology
Stem Cells
Neurobiology
Proteomics
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