FIBROTIC NON-HUMAN ANIMAL, AND USE THEREOF
|Posted date||May 18, 2020|
|International application number||2013JP079623|
|International publication number||WO 2014069597|
|Date of international filing||Oct 31, 2013|
|Date of international publication||May 8, 2014|
|Title||FIBROTIC NON-HUMAN ANIMAL, AND USE THEREOF|
|Abstract||The present invention provides a non-human animal IKKβ characterized by developing tissue fibrosis and being produced by deleting IKKβ gene in a myofibroblast- and/or smooth-muscle-cell-specific manner. The non-human animal develops a disease condition that is highly similar to scleroderma. Thus, the non-human animal can be used as a model animal for scleroderma and therefore is extremely useful.|
|Outline of related art and contending technology||
The deposition of collagen fibers is associated with tissue fibrosis, inflammatory response in vivo as a final image phenomenon occurs in the wound healing processes, such as wound is cured, to play an important role in vivo. On the other hand, the excessive tissue fibrosis, inflammation of a variety of diseases based, for example, skin diseases, heart disease, respiratory diseases, autoimmune disease, collagen disease, cancer, arteriosclerosis, diabetes and the like, of delaying the onset or exacerbation of the disease are factors. In addition, the mechanism of fibrosis is not a well - defined, fibrosis associated with the treatment of these diseases is difficult.
Collagen is one of scleroderma (systemic scleroderma) is, the synthesis of collagen fibers in the skin and enhance a visceral accumulation and mainly composed of a disease. The disease is characterized in that, in a ratio of about 1:9 men and women predominantly many, of the age is 30-50 is found in mid-age of twenties RVDS. In addition, the pathological condition is, Raynaud's symptoms, other skin lesions such as induration of the skin, pulmonary fibrosis, renal dysfunction, such as esophageal visceral disease also adversely affected. Therefore, quality of life as well as scleroderma, affects the life prognosis and intractable, current, or the like may also effective treatment has not been established.
Conventional, fibrosis, in animal models of scleroderma may be used as is, or drugs such as bleomycin (transforming growth factor beta) TGF β, CTGF (connective tissue growth factor), cytokines such as bFGF (basic fibroblast growth factor) artificially by administration of a mouse resulted in fibrosis (non-patent document 1, 2), or, due to genetic abnormality in the Tight skin mouse Fibrillin-1 (non-patent document 3, 4). However, these animal models is known, for example skin mice receiving cytokines locally at the site of administration to the skin and cures, male and female is about the same Tight skin mouse skin appreciably, esophageal renal failure or the like is not observed, such that there is a problem. Therefore, the model animal known scleroderma, similarity of both pathologies in human beings, and the like of the artificial surface may not be sufficient. In addition, in recent years Fibrillin-1 is scleroderma is completely different from the genetic disease Stiff Skin Syndrome is the causal genes has been reported (non-patent document 5) from the, scleroderma Tight skin mouse model mouse of the usefulness as a question has been developed.
|Scope of claims||
|IPC(International Patent Classification)|
National States: AE AG AL AM AO AT AU AZ BA BB BG BH BN BR BW BY BZ CA CH CL CN CO CR CU CZ DE DK DM DO DZ EC EE EG ES FI GB GD GE GH GM GT HN HR HU ID IL IN IR IS JP KE KG KN KP KR KZ LA LC LK LR LS LT LU LY MA MD ME MG MK MN MW MX MY MZ NA NG NI NO NZ OM PA PE PG PH PL PT QA RO RS RU RW SA SC SD SE SG SK SL SM ST SV SY TH TJ TM TN TR TT TZ UA UG US UZ VC VN ZA ZM ZW
ARIPO: BW GH GM KE LR LS MW MZ NA RW SD SL SZ TZ UG ZM ZW
EAPO: AM AZ BY KG KZ RU TJ TM
EPO: AL AT BE BG CH CY CZ DE DK EE ES FI FR GB GR HR HU IE IS IT LT LU LV MC MK MT NL NO PL PT RO RS SE SI SK SM TR
OAPI: BF BJ CF CG CI CM GA GN GQ GW KM ML MR NE SN TD TG
Contact Information for " FIBROTIC NON-HUMAN ANIMAL, AND USE THEREOF "
- Kyoto University Office of Society-Academia Collaboration for Innovation
- URL: https://www.saci.kyoto-u.ac.jp/
- Address: 36-1, Yoshida-honmachi, Sakyo-ku, Kyoto-shi, Kyoto, JAPAN , 606-8501
- Fax: +81-75-753-7591