New Therapeutic and Diagnostic Approaches for Liver Fibrosis
Tech ID: 21777 / UC Case 2011-295-0
Background
Hepatic fibroblasts are activated in response to chronic liver injury and are the source of the fibrous scar in liver fibrosis. Liver fibrosis is known to be reversible. It is thought that reversal of fibrosis is accompanied by senescence and/or apoptosis of the myofibroblasts, which are responsible for the fibrosis. However, it was unknown if myofibroblasts can escape cell death and revert to an inactive phenotype during regression of fibrosis.Technology Description
UC San Diego investigators have recently identified a cell sub-population called inactivated hepatic stellate cells (iHSCs), a type of myofibroblast thought to be reactivated during recurrent liver fibrosis. This phenotype is distinct from the other phenotypes heretofore thought to be involved in liver fibrosis. The inventors predict that by channeling activated hepatic stellate cells (aHSCs) toward inactivation (iHSCs) rather than apoptosis, or by keeping these iHSC cell types in an inactivated state, mitigation of liver fibrosis or prevention of its recurrence can be achieved.Targeting the aHSC cell type that is responsible for collagen production in liver fibrosis to go into an inactivated state, rather than targeting it for apoptosis, is a novel approach to treating liver fibrosis. These cells would be the target of anti-fibrotic therapy.
UC San Diego investigators have also determined that different myofibroblast activation pathways are responsible for different types of liver fibrosis. Some types of liver fibrosis originate mostly from hepatic stellate cells (HSCs). Other types of liver fibrosis disease block the common bile duct and involve mostly portal fibroblasts (PFs). By determining whether the type of liver fibrosis is caused principally by HSCs or by PFs, this method may have diagnostic applications to determine the most effective anti-fibrotic therapy.
The transgenic mice developed for this project could be useful as an animal model for any type of fibrosis study. Their advantage is that any individual mouse could be assayed at any point in time without sacrificing the mouse. Also, any type of collagen Type I fibrosis could be studied in these mice, including cardiovascular, pulmonary, kidney, or cystic fibrosis. While not a high throughput system, the mice could be a secondary screening for therapeutic agents for anti-fibrotic drugs.
Intellectual Property Info
United States patent rights are available for licensing. UC San Diego is seeking a commercial partner for this technology.Related Materials
- Kisseleva T, Paik Y, Scholten D, Fanli Meng F, Iwaisako K, Jiang C, Brenner DA. Hepatic Stellate Cells revert to an inactive phenotype during regression of Fibrosis. Poster presentation at The Liver Meeting, September 2010 (Amer. Assoc. for the Study of Liver Disease)
- Kisseleva T, Paik Y, Scholten D, Fanli Meng F, Iwaisako K, Jiang C, Brenner DA. Hepatic Stellate Cells revert to an inactive phenotype during regression of Fibrosis. Gastroenterology Vol. 140, Issue 5, Supplement 1, Pages S-916-S-917.
Patent Status
| Country | Type | Number | Dated | Case |
| United States Of America | Published Application | 13/0101553 | 04/25/2013 | 2011-295 |
Other Information
Categorized As
Related cases
2011-295-0, 2011-296-0
Contact
University of California, San Diego Technology Transfer Office / invent@ucsd.edu / tel: View Phone Number. Please reference Tech ID #21777.