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Substrate stiffness engineered to replicate disease conditions influence senescence and fibrotic responses in primary lung fibroblasts.
- Published in:
- Frontiers in Pharmacology, 2022, v. 13, p. 1, doi. 10.3389/fphar.2022.989169
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- Article
Senescence of IPF Lung Fibroblasts Disrupt Alveolar Epithelial Cell Proliferation and Promote Migration in Wound Healing.
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- Pharmaceutics, 2020, v. 12, n. 4, p. 389, doi. 10.3390/pharmaceutics12040389
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- Article
Mitochondrial dysfunction contributes to the senescent phenotype of IPF lung fibroblasts.
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- Journal of Cellular & Molecular Medicine, 2018, v. 22, n. 12, p. 5847, doi. 10.1111/jcmm.13855
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- Article
A Senescence Bystander Effect in Human Lung Fibroblasts.
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- Biomedicines, 2021, v. 9, n. 9, p. 1162, doi. 10.3390/biomedicines9091162
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- Article
Regulation of Cellular Senescence Is Independent from Profibrotic Fibroblast-Deposited ECM.
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- Cells (2073-4409), 2021, v. 10, n. 7, p. 1628, doi. 10.3390/cells10071628
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- Article
Regulation of cellular senescence by extracellular matrix during chronic fibrotic diseases.
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- Clinical Science, 2020, v. 134, n. 20, p. 2681, doi. 10.1042/CS20190893
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- Article
Self DNA perpetuates IPF lung fibroblast senescence in a cGAS-dependent manner.
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- Clinical Science, 2020, v. 134, n. 7, p. 889, doi. 10.1042/CS20191160
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- Article