
Non cell autonomous upregulation of CDKN2 transcription linked to progression of chronic hepatitis C disease
Author(s) -
Robinson Mark W.,
McGuinness Dagmara,
Swann Rachael,
Barclay Stephen,
Mills Peter R.,
Patel Arvind H.,
McLauchlan John,
Shiels Paul G.
Publication year - 2013
Publication title -
aging cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.103
H-Index - 140
eISSN - 1474-9726
pISSN - 1474-9718
DOI - 10.1111/acel.12125
Subject(s) - biology , telomere , downregulation and upregulation , locus (genetics) , senescence , biomarker , disease , hepatitis c virus , immunology , cancer research , virology , genetics , virus , gene , medicine
Summary Chronic hepatitis C virus infection (C‐ HC ) is associated with higher mortality arising from hepatic and extrahepatic disease. This may be due to accelerated biological aging; however, studies in C‐ HC have thus far been based solely on telomere length as a biomarker of aging (BoA). In this study, we have evaluated CDKN 2 locus transcripts as alternative BoAs in C‐ HC . Our results suggest that C‐ HC induces non‐cell‐autonomous senescence and accelerates biological aging. The CDKN 2 locus may provide a link between C‐ HC and increased susceptibility to age‐associated diseases and provides novel biomarkers for assessing its impact on aging processes in man.