Revolutionizing Lung Transplants: UVA Researchers Uncover Key Insights to Boost Survival Rates

“Potential Breakthrough in Lung Transplantation: Improving Survival Rates Explored by University of Virginia School of Medicine Researchers”

Researchers at the University of Virginia School of Medicine have uncovered a promising avenue to enhance the survival rates of lung transplant patients. In cases of advanced or end-stage respiratory diseases, lung transplants often stand as the sole treatment option. Despite recent improvements in patient survival rates post-transplant, they still significantly trail behind those observed in other organ transplant procedures, prompting doctors and researchers to seek ways to refine the process and mitigate post-transplant complications.

Under the leadership of Swapnil K. Sonkusare from UVA’s Department of Molecular Physiology and Biological Physics, a team has identified cellular changes within the transplanted lung that contribute to “ischemia-reperfusion injury.” This injury, a major cause of organ rejection and post-transplant mortality, occurs when blood supply returns to tissue after a period without oxygen.

Sonkusare and his team propose that targeting these underlying biological processes could potentially prevent ischemia-reperfusion injuries. Their findings, published in the journal Science Signaling, highlight a new mechanism for lung ischemia-reperfusion injury through collaborative studies with
Dr. Victor Laubach affiliated with the Department of Surgery at the University of Virginia (UVA). Ischemia-reperfusion injury plays a pivotal role in “primary graft dysfunction,” the leading cause of death within 30 days of a lung transplant, and can also lead to chronic allograft dysfunction, the primary cause of death a year or more after transplantation. Approximately half of lung transplant recipients develop chronic allograft dysfunction within five years, according to the National Institutes of Health.

While some degree of ischemia-reperfusion injury is inevitable in organ transplant recipients, the trauma experienced by tissues during the disconnection from the original blood supply and reconnection to a new one can result in harmful inflammation, leaky blood vessels, damage to oxygen-exchange sacs, and other complications.

Although the phenomenon of ischemia-reperfusion injury is well-known, understanding its underlying causes has proven challenging. Sonkusare’s recent work offers valuable insights, pinpointing a specific pathway of biological processes triggered by ischemia-reperfusion in endothelial cells lining blood vessels in the lung. This activation leads to immune cell activation and subsequent lung injury.

Blocking key steps in this pathway in lab mice demonstrated prevention of inflammation and lung damage, suggesting a promising approach for averting similar problems in human transplant recipients. However, extensive research is still required to validate the effectiveness of drug molecules in enhancing the success rate of lung transplantation.

Dr. Sonkusare emphasized ongoing collaborative efforts with Dr. Laubach in unraveling cellular mechanisms for lung ischemia-reperfusion injury. The team is actively testing drug molecules to block these mechanisms in various models of lung injury after transplantation, with the ultimate goal of improving the success rate of lung transplantation.

 

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