Aug 21, 2019

Age-related clonal haemopoiesis is associated with increased epigenetic age

Current Biology : CB
Neil A RobertsonTamir Chandra

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.

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Mentioned in this Paper

Hematologic Neoplasms
TET2 gene
Cardiovascular Diseases
X Chromosome
Clone
Methylation
Archease protein, human
Atherosclerosis
Chronic Myocardial Ischemia
DNMT3A gene

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