It is of great theoretical and practical value to establish disease models with mice and other model animals. On the one hand, the analysis of gene function and inheritance mode through animal model research has become the main driving force to promote the important theoretical achievements of life science. For example, the mutant phenotype analysis of Drosophila and the functional study of mouse-related genes directly led to the establishment of the basic framework of multicellular biological development theory. On the other hand, the in-depth study of animal models, especially mouse disease models, will bring great business opportunities to the biomedical technology industry. Almost all new mouse models, especially animal models of cardiovascular diseases, metabolic diseases and senile diseases that seriously endanger human health, have been patented. Taking the latest research results of mouse database as an example, the researchers obtained more than 30 mutant strains of mice by ENU mutation method, including cataract, deafness, abnormal bone density, limb defects and hair abnormalities, and cloned some related mutant genes. These mutant genes will find new drug targets for the treatment of these diseases, and these models may be used for the screening and development of new drugs. Using gene knockout technology, the researchers also established a series of mutant mouse models, such as abnormal bone development, embryonic development defects, abnormal blood sugar regulation, and defective immune cell differentiation, which provided a basis for the pathogenesis research and drug development of diseases such as genetic diseases with developmental defects, diabetes and lymphoma.
Mouse model can not simulate human inflammatory diseases well.
For decades, experimental mouse models have been used to identify and test candidate drugs before human trials, but a study found that these models cannot accurately represent human responses to inflammatory diseases. Junhee Seok and his colleagues studied how trauma, burns and toxins from bacteria such as Escherichia coli affect the genetic response of patients. Then, the author compares the observed patterns with those observed in the mouse model. The author thinks that the patterns of these mouse models don't match the human response patterns, so the results seem to be random. The evolutionary distance between humans and mice, the obvious resistance of mice to inflammatory stimuli and other factors may explain why these models can not reproduce the human situation. The author calls on biomedical research methods to pay attention to how human physiology and diseases affect human beings at molecular and genetic levels, rather than relying mainly on mouse models. A promising discovery is that patients with inflammation due to trauma, burns or other diseases show similar genetic reactions, although the causes of these diseases are completely different and these patients have received different treatments. The authors say that these findings also show that many drugs for different inflammatory diseases may bring improved treatment to a large number of patients.
The completion of the human genome project and the continuous establishment of disease models once again emphasize the importance of independent intellectual property rights. Just cloning a new gene is not enough to apply for a patent. The understanding of gene function has become the main content of the new round of biomedical intellectual property market. Although many domestic units have cloned a large number of genes through gene chips, they are unable to seize the patent market due to the lack of support for functional research, especially the most powerful functional research results like mouse models.