Mice which are +/− or −/− for the elastin gene as models for vascular disease
US6903244B1 · kind B1 · utility
Assignee
Inventors
Key dates
| Filing date | Feb 26, 1999 |
| Grant date | Jun 7, 2005 |
| Priority date | — |
| Expiry date | Feb 26, 2019 |
Classification
- Technology area (CPC A)Human Necessities
- CPC primaryA61P9/10
- WIPO fieldPharmaceuticals
- WIPO sectorChemistry
Abstract
Elastin, the main component of arterial extracellular matrix, was thought to have a purely structural role. Consistent with this view, elastin hemizygous mice maintain arterial extensibility by increasing the number of elastic lamellae during development. However, mice lacking elastin die of obstructive arterial pathology. This pathology results from subendothelial proliferation and reorganization of smooth muscle, cellular changes similar to those observed in atherosclerosis. Thus, elastin is a molecular determinant of arterial morphogenesis and likely plays a central role in vascular disease. Mice which are heterozygous and null for the elastin gene have been developed. These mice are extremely useful for screening for drugs useful for treating persons with atherosclerosis, hypertension, SVAS or other vascular diseases.
Source: USPTO / EPO open patent data. Objective bibliographic and citation counts.