Shared first authors.
Non cell autonomous upregulation of CDKN2 transcription linked to progression of chronic hepatitis C disease
Article first published online: 12 AUG 2013
© 2013 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Volume 12, Issue 6, pages 1141–1143, December 2013
How to Cite
Robinson, M. W., McGuinness, D., Swann, R., Barclay, S., Mills, P. R., Patel, A. H., McLauchlan, J. and Shiels, P. G. (2013), Non cell autonomous upregulation of CDKN2 transcription linked to progression of chronic hepatitis C disease. Aging Cell, 12: 1141–1143. doi: 10.1111/acel.12125
This research was supported by funding from the UK Medical Research Council (MRC).
- Issue published online: 21 NOV 2013
- Article first published online: 12 AUG 2013
- Accepted manuscript online: 26 JUN 2013 12:50PM EST
- Manuscript Accepted: 16 JUN 2013
- UK Medical Research Council
- biological aging;
- CDKN2 locus;
- chronic HCV infection;
- telomere length
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 CDKN2 locus transcripts as alternative BoAs in C-HC. Our results suggest that C-HC induces non-cell-autonomous senescence and accelerates biological aging. The CDKN2 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.