Gene expression analysis reveals matrilysin as a key regulator of pulmonary fibrosis in mice and humans
By F. Zuo, Naftali Kaminski, E. Eugui, J. Allard, Zohar Yakhini, A. Ben-Dor, L. Lollini, David G. Morris, Y. Kim, B. Delustro and 4 more. Proceedings of the National Academy of Sciences of the United States of America, 2002
619 citations recorded by the source corpus.
Subfields: Cardiology and Cardiovascular Medicine, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/55abf7a8d04f2998f8da674efc84d9f0cf938a84
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cardiology and Cardiovascular Medicine
In Pulmonary and Respiratory Medicine
Citations in the corpus
- Matrix metalloproteinase inhibitors as therapy for inflammatory and vascular diseases (2007, background): “Mmp7 was found to be one of the most upregulated genes in the lungs of bleomycin-treated mice, and Mmp7 -knockout mice were less sensitive to the induced fibrosi”
- Integrating mechanisms of pulmonary fibrosis (2011, background): “They promote fibrosis by secreting chemokines and specific matrix metalloproteinases that degrade ECM components, thus facilitating the recruitment of inflammatory cells to sites of tissue injury (Zuo et al., 2002; Jiang et al., 2005).”
- Matrilysin shedding of syndecan-1 regulates chemokine mobilization and transepithelial efflux of neutrophils in acute lung injury. (2002, positive): “Elevated myeloperoxidase levels in lung homogenates did not differ between SYN1 / Recently, two groups reported that matrilysin is prominently expressed by the epithelium in human pulmonary and WT bleomycin-instilled mice were similar (data not shown) indicating that neutrophil movement into the fib”