DOI . ORG {
}
We began analyzing https://link.springer.com/article/10.1007/s11926-009-0017-1, but it redirected us to https://link.springer.com/article/10.1007/s11926-009-0017-1. The analysis below is for the second page.
Title[redir]:
Tissue stiffness, latent TGF-β1 Activation, and mechanical signal transduction: Implications for the pathogenesis and treatment of fibrosis | Current Rheumatology Reports
Description:
Tissue stiffening is a predominant feature of fibrosis and it obstructs organs whose mechanical properties are important for their function, such as the heart, lung, skin, and vessels. Stiff scar tissue further modulates the character of the healthy residing cells by driving the differentiation of a variety of precursor cells into fibrogenic myofibroblasts. This mechanical cue for myofibroblast differentiation establishes a vicious cycle because the excessive extracellular matrix-secreting and remodeling activities of myofibroblasts are cause and effect of further connective tissue contracture and stiffening. The second pivotal factor inducing myofibroblast development is transforming growth factor-β1. Recent findings suggest that transforming growth factor-β1 activity is partly controlled by myofibroblast contractile forces and tissue stiffness. This discovery opens new paths to prevent progression of fibrosis by specifically interfering with the stress perception and transmission mechanisms of the myofibroblast.
Title[redir]:
Tissue stiffness, latent TGF-β1 Activation, and mechanical signal transduction: Implications for the pathogenesis and treatment of fibrosis | Current Rheumatology Reports
Description:
Tissue stiffening is a predominant feature of fibrosis and it obstructs organs whose mechanical properties are important for their function, such as the heart, lung, skin, and vessels. Stiff scar tissue further modulates the character of the healthy residing cells by driving the differentiation of a variety of precursor cells into fibrogenic myofibroblasts. This mechanical cue for myofibroblast differentiation establishes a vicious cycle because the excessive extracellular matrix-secreting and remodeling activities of myofibroblasts are cause and effect of further connective tissue contracture and stiffening. The second pivotal factor inducing myofibroblast development is transforming growth factor-β1. Recent findings suggest that transforming growth factor-β1 activity is partly controlled by myofibroblast contractile forces and tissue stiffness. This discovery opens new paths to prevent progression of fibrosis by specifically interfering with the stress perception and transmission mechanisms of the myofibroblast.
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Keywords {🔍}
article, pubmed, google, scholar, cas, cell, fibrosis, biol, tissue, activation, growth, myofibroblast, hinz, tgfbeta, transforming, cancer, matrix, latent, mechanical, mesenchymal, cells, differentiation, stem, privacy, cookies, content, stiffness, lung, access, pathol, fibroblasts, muscle, int, rev, sci, publish, search, implications, pathogenesis, myofibroblasts, extracellular, factor, mechanisms, invest, res, kidney, disease, factorbeta, integrin, alphavbeta,
Topics {✒️}
transforming growth factor-β1 integrin-mediated tgf{beta}1 activation month download article/chapter alpha-smooth muscle actin latent tgf-{beta} requires adult stem/progenitor cells latent tgf-β1 activation tgf{beta}1-null mice alphavbeta6 integrin-dependent mechanisms mesenchymal stem cell myofibroblast contractile forces excessive extracellular matrix-secreting connective tissue contracture epithelial-mesenchymal transition {beta}6-mediated activation stem-cell therapy stiff scar tissue full article pdf integrin-mediated activation rho signaling pathway tissue stiffness 3d collagen matrices mechanical tension stimulates normal tissue repair privacy choices/manage cookies invasive cancer growth human burn scars article hinz healthy residing cells myofibroblast force perception integrin alphavbeta5 induces tgf-beta rigidity inhibits beating collagen4a3-deficient mice antibody-mediated blockade mechanical signal transduction maintaining epithelial homeostasis integrin {alpha} integrin alpha european economic area coronary artery lesion embryonic cardiomyocytes beat cutaneous wound healing decreased cellular apoptosis acute lung injury myofibroblast differentiation establishes conditions privacy policy boris hinz recent findings suggest stress perception
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headline:Tissue stiffness, latent TGF-β1 Activation, and mechanical signal transduction: Implications for the pathogenesis and treatment of fibrosis
description:Tissue stiffening is a predominant feature of fibrosis and it obstructs organs whose mechanical properties are important for their function, such as the heart, lung, skin, and vessels. Stiff scar tissue further modulates the character of the healthy residing cells by driving the differentiation of a variety of precursor cells into fibrogenic myofibroblasts. This mechanical cue for myofibroblast differentiation establishes a vicious cycle because the excessive extracellular matrix-secreting and remodeling activities of myofibroblasts are cause and effect of further connective tissue contracture and stiffening. The second pivotal factor inducing myofibroblast development is transforming growth factor-β1. Recent findings suggest that transforming growth factor-β1 activity is partly controlled by myofibroblast contractile forces and tissue stiffness. This discovery opens new paths to prevent progression of fibrosis by specifically interfering with the stress perception and transmission mechanisms of the myofibroblast.
datePublished:2009-03-22T00:00:00Z
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Chymal Stem Cell
Contractile Stress
Rheumatology
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headline:Tissue stiffness, latent TGF-β1 Activation, and mechanical signal transduction: Implications for the pathogenesis and treatment of fibrosis
description:Tissue stiffening is a predominant feature of fibrosis and it obstructs organs whose mechanical properties are important for their function, such as the heart, lung, skin, and vessels. Stiff scar tissue further modulates the character of the healthy residing cells by driving the differentiation of a variety of precursor cells into fibrogenic myofibroblasts. This mechanical cue for myofibroblast differentiation establishes a vicious cycle because the excessive extracellular matrix-secreting and remodeling activities of myofibroblasts are cause and effect of further connective tissue contracture and stiffening. The second pivotal factor inducing myofibroblast development is transforming growth factor-β1. Recent findings suggest that transforming growth factor-β1 activity is partly controlled by myofibroblast contractile forces and tissue stiffness. This discovery opens new paths to prevent progression of fibrosis by specifically interfering with the stress perception and transmission mechanisms of the myofibroblast.
datePublished:2009-03-22T00:00:00Z
dateModified:2009-03-22T00:00:00Z
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pageEnd:126
sameAs:https://doi.org/10.1007/s11926-009-0017-1
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Tissue Stiffness
Latency Associate Peptide
Chymal Stem Cell
Contractile Stress
Rheumatology
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