Non cell autonomous upregulation of CDKN2 transcription linked to progression of chronic hepatitis C disease

Aging Cell

Mark W. Robinson⁴  Dagmara McGuinness¹  Rachael Swann⁴  Stephen Barclay²  Peter R. Mills³  Arvind H. Patel⁴  John McLauchlan⁴ 

[1] Section of Epigenetics, Institute of Cancer Sciences, MVLS, University of Glasgow, Glasgow, UK;Glasgow Royal Infirmary, NHS Greater Glasgow and Clyde, Glasgow, UK;Gartnavel General Hospital, NHS Greater Glasgow and Clyde, Glasgow, UK;MRC – University of Glasgow Centre for Virus Research, Glasgow, UK

关键词: biological aging;    CDKN2 locus;    chronic HCV infection;    telomere length;   

DOI  :  10.1111/acel.12125

来源: Wiley

【 摘 要 】

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 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.

【 授权许可】

CC BY   
© 2013 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.

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