Regulation of lung injury and repair by Toll-like receptors and hyaluronan

By D. Jiang, Jiurong Liang, Juan Fan, Shuang Yu, Suping Chen, Yi Luo, G. Prestwich, Marcella M. Mascarenhas, H. Garg, D. Quinn and 6 more. Nature Medicine, 2005

1,456 citations recorded by the source corpus.

Subfields: Cell Biology, Immunology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/00b4ca23e089493c7d5c999aa67fbee82db2aca2

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

1. R. Medzhitov
2. K. Girish
3. P. Saftig
4. S. Eming
5. TA Wynn
6. K. Kemparaju
7. S. Amigorena
8. Nikolaos G. Frangogiannis

In Immunology

1. R. Medzhitov
2. L. Zitvogel
3. E. Latz
4. TA Wynn
5. R. Coffman
6. F. Barrat
7. H. Kanzler
8. E. Hessel

In Pulmonary and Respiratory Medicine

1. TA Wynn
2. P. Noble
3. Jeremy S. Duffield

Citations in the corpus

• Hyaluronan as an Immune Regulator in Human Diseases (2011, positive): “We found that bleomycin induces both NF- B activation and apoptosis in primary lung epithelial cells (185).”
• Origin and physiological roles of inflammation (2008, background): “Tissue injury promotes its breakdown into low-molecular-weight fragments, which are inflammatory, activating TLR4 and promoting a tissue-repair respons”
• Toll-like receptor 4–dependent contribution of the immune system to anticancer chemotherapy and radiotherapy (2007, background): “: heat-shock protein (HSP) 60, HSP70, oxidized LDL, surfactant protein A, hyaluronan breakdown product”
• The magic glue hyaluronan and its eraser hyaluronidase: a biological overview. (2007, background): “Recent studies confirmed that HA oligomers require MyD88 and both toll like receptor 4 (TLR4) and TLR2 in vitro and in vivo to initiate the inflammatory response in acute lung injury (Jiang et al., 2005).”
• The sterile inflammatory response (2010, background): “Similarly, released cellular proteases can cleave extracellular matrix components into bioactive fragments (52) .”
• 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).”
• Para-inflammation in the aging retina. (2009, background): “Oligosaccharides of HAs are pro-inflammatory and induce cytokine/chemokine (McKee et al., 1996; Noble et al., 1996) production in macrophages via TLR2/TLR4 receptors (Jiang et al., 2005).”
• TLR4 and CD14 trafficking and its influence on LPS-induced pro-inflammatory signaling (2020, background): “These compounds are released during tissue injury and can activate TLR4 in non-infectious conditions to induce tissue repair [7, 8].”