Study finds protein which could prevent multi-organ failure in patients with acute liver disease

New Delhi, Nov 14 (PTI) Scientists have discovered a protein in the immune system, manipulating which could offer a possibility to prevent multi-organ failure in patients with severe liver injury.

Researchers explained that damage in one part of the body triggers ageing and failure in cells, which can spread to other organs.

Senescence, in which cells become tired and stop working effectively, is a common effect of ageing, but can also be triggered due to disease at any stage of life.

Senescence in liver cells because of acute disease can cause irreparable damage, leading to the organ's failure and potentially triggering multi-organ failure.

In mice and liver tissues taken from humans having acute liver disease, the researchers, led by those at the University of Edinburgh, UK, found that once a large enough number of liver cells were damaged, senescence started to appear in other organs, including kidneys and lungs, thereby increasing the risk of multi-organ failure and need for liver transplantation.

The team also identified a biological process involving 'TGFβ', a protein related to the immune system, blocking the activity of which was found to prevent the damage in liver cells from spreading to other organs.

The findings, published in the journal Nature Cell Biology, provide the first insight into why severe liver injury results in the failure of other organs, such as the brain and kidneys, and death, study author Rajiv Jalan, a professor of hepatology at the University College London, UK, said.

"We were able to validate these novel and exciting observations in patients, providing a route to develop biomarkers that can be measured in the blood to identify those at risk, and new therapies to treat severe liver disease," Jalan said.

While there is currently no test to predict how a sudden liver failure will progress, monitoring liver cells could help identify those most at risk, including those likely to need a transplant, the researchers said.

"We identify the TGFβ pathway as a critical mediator of systemic spread of senescence and demonstrate that TGFβ inhibition (in body) blocks senescence transmission to other organs, preventing liver senescence-induced renal (kidney) dysfunction," the authors wrote. PTI KRS ARI