'Protective switch' proteins could enhance liver transplant success by reducing damage

New research identifies proteins that act as protective switches in the liver, potentially increasing the success and availability of transplants by reducing ischemia-reperfusion injury.
Researchers at the University of California, Los Angeles, have discovered that certain proteins act as 'protective switches' in the liver, shielding it from damage during the transplantation process. This damage, known as ischemia-reperfusion injury, occurs when blood supply to the liver is temporarily cut off and then reestablished, often causing inflammation and organ injury. Using a mouse model, the team identified proteins like CEACAM1 and Human Antigen R (HuR) that work together to prevent this type of damage.
The significance of this discovery lies in its potential to increase the availability of donor livers. Currently, many organs are discarded due to damage that occurs during transplantation, limiting the donor pool. By utilizing molecular therapies to activate these protective proteins, damaged organs could be strengthened and deemed suitable for transplantation, ultimately saving more lives.
The research revealed that boosting HuR and CEACAM1 levels in mice reduced liver injury. Interestingly, similar protective relationships were observed in discarded human livers, suggesting possible applications in clinical settings. Despite these promising findings, the researchers caution that further studies are needed to confirm whether these protective mechanisms can be effectively activated in human organs prior to transplant.
Next steps involve testing methods to turn on these protective switches in whole human organs kept alive outside the body. If successful, such approaches could revolutionize liver transplantation practices, making procedures safer and increasing organ availability, thereby decreasing patient mortality rates while waiting for transplants.
Published in JCI Insight, this study offers new hope for addressing the persistent shortage of donor livers and improving long-term transplant outcomes.
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