Mechanosensing by the α 6-integrin confers an invasive fibroblast phenotype and mediates lung fibrosis
Nature Communications, ISSN: 2041-1723, Vol: 7, Issue: 1, Page: 12564
2016
- 124Citations
- 103Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations124
- Citation Indexes124
- 124
- CrossRef71
- Captures103
- Readers103
- 103
Article Description
Matrix stiffening is a prominent feature of pulmonary fibrosis. In this study, we demonstrate that matrix stiffness regulates the ability of fibrotic lung myofibroblasts to invade the basement membrane (BM). We identify α 6-integrin as a mechanosensing integrin subunit that mediates matrix stiffness-regulated myofibroblast invasion. Increasing α 6-expression, specifically the B isoform (α 6 B), couples β 1-integrin to mediate MMP-2-dependent pericellular proteolysis of BM collagen IV, leading to myofibroblast invasion. Human idiopathic pulmonary fibrosis lung myofibroblasts express high levels of α 6-integrin in vitro and in vivo. Genetic ablation of α 6 in collagen-expressing mesenchymal cells or pharmacological blockade of matrix stiffness-regulated α 6-expression protects mice against bleomycin injury-induced experimental lung fibrosis. These findings suggest that α 6-integrin is a matrix stiffness-regulated mechanosensitive molecule which confers an invasive fibroblast phenotype and mediates experimental lung fibrosis. Targeting this mechanosensing α 6 (β 1)-integrin offers a novel anti-fibrotic strategy against lung fibrosis.
Bibliographic Details
Springer Science and Business Media LLC
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