Galectin-3 regulates myofibroblast activation and hepatic fibrosis.

By N. Henderson, A. MacKinnon, Sarah L. Farnworth, F. Poirier, F. Russo, J. Iredale, C. Haslett, K. Simpson, T. Sethi. Proceedings of the National Academy of Sciences of the United States of America, 2006

622 citations recorded by the source corpus.

Subfields: Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/b06e0a0c293f8cf714445fe6c1d9c5482f30207c

How researchers see this paper

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

In Immunology

1. B. Hinz
2. Weimin He

In Oncology

1. B. Hinz
2. Weimin He

Citations in the corpus

• Galectin-3, a Marker of Cardiac Fibrosis, Predicts Incident Heart Failure in the Community (2012, background): “fibrosis but also other fibrotic conditions, including liver cirrhosis (29,30) and pulmonary fibrosis (31), all of which could increase the risk for overall mortality.”
• Formation and function of the myofibroblast during tissue repair. (2007, background): “Binding of galectin-3 to growth factor receptors has been demonstrated but its cooperation with TGFb1 is not yet understood (Henderson et al., 2006).”
• RNA silencing: Methods and protocols (2006, positive): “Disruption of the galectin-3 gene blocked myofibroblast activation and procollagen expression in vitro and in vivo, and addition of exogenous recombinant galectin-3 in vitro reversed this abnormality [46].”
• Selective αv integrin depletion identifies a core, targetable molecular pathway that regulates fibrosis across solid organs (2013, neutral): “Paraffin-embedded sections were processed for immunohistochemistry as described previously 47 .”