[Airway remodeling in asthma].
By R. Zagdańska, I. Grzelewska-Rzymowska. Pneumonologia i Alergologia Polska, 2003
798 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/f9173ef7dafe9b91f2439e3b4cb297c824ba5dc7
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Citations in the corpus
- Thymic stromal lymphopoietin as a key initiator of allergic airway inflammation in mice (2005, background): “The hallmarks of the disease include infiltration of the airways by leukocytes, varying degrees of subepithelial fibrosis, mucus hyperproduction, hypertrophy and hyperplasia of smooth muscle, goblet cell hyperplasi”
- The comet assay: a method to measure DNA damage in individual cells (2006, background): “When coupled with cytokines, inflammatory cells or mechanical stress, the airway wall model responds in ways that mimic human pathophysiology, including cytokine upregulation, myofibroblast differentiation and matrix remodelin”
- Interleukin-13 Induces Tissue Fibrosis by Selectively Stimulating and Activating Transforming Growth Factor β1 (2001, background): “This is based on studies from our laboratory that demonstrated that the transgenic overexpression of IL-13 in the murine airway causes subepithelial airway fibrosis that is similar, in many ways, to the fibrotic response seen in remodeled human asthmatic airways (3, 25).”
- Increased airway epithelial Na+ absorption produces cystic fibrosis-like lung disease in mice (2004, background): “In contrast to mouse models of allergic airway diseas”
- Role of Chitin and Chitinase/Chitinase-Like Proteins in Inflammation, Tissue Remodeling, and Injury (2011, background): “Type 2 cytokine– producing cells are now believed to be major contributors to the initiation and maintenance of airway inflammation, the regulation of B cell and eosinophil function, the induction of mucus, and the stimulation of remodeling (91, 92).”
- Identification of Circulating Fibrocytes as Precursors of Bronchial Myofibroblasts in Asthma1 (2003, background): “The remodeling process has become an important target for therapeutic intervention (3, 5) because it may contribute to the chronic sequelae of asthma (6, 7), leading to permanently impaired pulmonary function and work disability (8).”