Robertson, N.A. and Hillary, R.F. and McCartney, D.L. and Terradas-Terradas, M. and Higham, J. and Sproul, D. and Deary, I.J. and Kirschner, K. and Marioni, R.E. and Chandra, T. (2019) Age-related clonal haemopoiesis is associated with increased epigenetic age. Current Biology, 29 (16). R786-R787. ISSN 0960-9822
Full text not available from this repository.Abstract
Age-related clonal haemopoiesis (ARCH) in healthy individuals was initially observed through an increased skewing in X-chromosome inactivation [1]. More recently, several groups reported that ARCH is driven by somatic mutations [2], with the most prevalent ARCH mutations being in the DNMT3A and TET2 genes, previously described as drivers of myeloid malignancies. ARCH is associated with an increased risk for haematological cancers [2]. ARCH also confers an increased risk for non-haematological diseases, such as cardiovascular disease, atherosclerosis, and chronic ischemic heart failure, for which age is a main risk factor 3, 4. Whether ARCH is linked to accelerated ageing has remained unexplored. The most accurate and commonly used tools to measure age acceleration are epigenetic clocks: they are based on age-related methylation differences at specific CpG sites [5]. Deviations from chronological age towards an increased epigenetic age have been associated with increased risk of earlier mortality and age-related morbidities 5, 6. Here we present evidence of accelerated epigenetic age in individuals with ARCH.