Galectin Therapeutics Inc. (GALT)

[staccani]

CONCLUSION
Here we have strived to present the role of cell death in liver disease, and propose that while apoptosis may not be the root cause of liver diseases, preventing liver cell death would mitigate the pathology and improve health in the majority of disease states. Decreased hepatocyte cell death would mitigate the need for continued regeneration. While the liver is quite famous for its regenerative capacity, in the healthy state very little hepatocyte cell division is seen. The chronic death and replacement of hepatocytes contributes to the proliferative and inflammatory environment in the cirrhotic liver, ultimately resulting in malignancy in some. In acute liver disease, the link between liver injury and loss of liver synthetic, metabolic, and secretory function becomes more pronounced. Here again, prevention of hepatocyte cell death would decrease disease severity, allowing for regeneration and restoration of liver function and mass without the need for transplantation. Be it due ethanol, BAs, or xenobiotics, cell death plays a role in their effects. Inflammatory states of the liver have a particularly insidious ability to be self-reinforcing, where inflammation induces cell death, resulting in activation of Kupffer cell-derived cytokines that further amplify the inflammation. As the liver is the first line of defense for detoxification, plays a role in innate immunity, and features prominently in hemostasis and normoglycemia, preventing damage to the various cell types of the liver is an important goal to maintain health not only of the liver, but of its owner.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3867948/