EASL 2015: CNIO Researchers Link Telomeres to the Origins of Liver Diseases such as Chronic Hepatitis and Cirrhosis

• Researchers have generated a mouse with dysfunctional telomeres in the liver and, as a result, it developed cellular alterations present in human diseases such as hepatitis or cirrhosis
• This study is the first to show that alterations in the functioning of telomeres lead to changes in the liver that are common to diseases such as hepatitis and cirrhosis, which are associated with an increased risk of liver cancer
• This finding provides the basis for understanding the molecular origin of these diseases, as well as identifying new therapeutic strategies for their prevention and control

Madrid (Spain), April 16, 2015. Telomeres are DNA regions at the ends of our chromosomes that protect the genetic data of cells, preventing mutations and alterations in the DNA that could potentially cause disease. Telomeres shorten throughout life in a process involving both genetic and environmental factors. Telomere dysfunction —alterations in the structure and/or functioning of telomeres— is one of the molecular mechanisms underlying a number of age-related diseases but, to date, little is known about its possible role in pathologies of the liver such as cirrhosis, hepatitis and liver cancer.

In a study published in the Journal of Hepatology, Fabian Beier and Paula Martínez —from the Spanish National Cancer Research Centre´s (CNIO) Telomere and Telomerase Group led by Maria Blasco— have created a mouse model that recapitulates the origin of human diseases associated with long-term or chronic liver damage, such as hepatitis or cirrhosis of the liver which, in turn, can progress to liver cancer over time. This new mouse model reveals telomeric dysfunction as a potential factor in triggering these diseases.

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