Telomere Length in Patients with Alcohol-Associated Liver Disease: A Brief Report

Abstract

The intact telomere structure is essential for the prevention of the chromosome end-to-end fusions and maintaining genomic integrity. The maintenance of telomere length is critical for cellular homeostasis. The shortening of telomeres has been reported in patients with chronic liver diseases. The telomere length has not been systemically studied in patients with alcohol-associated liver disease (ALD) at different stages, such as alcoholic hepatitis and alcoholic cirrhosis. In this brief report, we observed evidence of telomere shortening without changes in the telomerase activity in the liver of patients with alcoholic hepatitis and alcoholic cirrhosis when compared with controls. The alterations in the genes associated with telomere binding proteins were only observed in patients with alcoholic cirrhosis. Future studies are required to determine the mechanism of how alcohol affects the length of the telomere and if the shortening impacts the disease progression in ALD.

Telomere dysfunction promotes cholangiocyte senescence and biliary fibrosis in primary sclerosing cholangitis

“…In pulmonary fibrosis, alveolar epithelial cells lacking Tert develop senescence and perpetuate the fibrotic phenomena in the lungs ( 23 ). Telomere shortening has been demonstrated in several liver diseases, including primary biliary cholangitis, NAFLD, and alcoholic liver disease ( 16 , 18 , 24 – 27 ). Although peripheral blood analysis of telomere length in patients with PSC reveals shorter telomeres ( 28 ), whether this reflects telomere dysfunction in liver tissue and in cholangiocytes has not been studied.…”

“…In pulmonary fibrosis, alveolar epithelial cells lacking Tert develop senescence and perpetuate the fibrotic phenomena in the lungs (23). Telomere shortening has been demonstrated in several liver diseases, including primary biliary cholangitis, NAFLD, and alcoholic liver disease (16,18,(24)(25)(26)(27).…”