LAUSR

Description Spread of Y chromosome aneuploidy in myeloid cells with age promotes cardiac fibrosis During their lifetimes, organisms acquire somatic mutations in individual cells caused by genomic instability, endogenous DNA replication errors, or exposure to mutagens (1). When mutations occur in somatic stem cells, the mutation “spreads” in a mosaic manner, appearing in the progeny of mutated stem cells but not in cells from nonmutated stem cells. Mosaic loss of Y chromosome (mLOY) has been observed in peripheral leukocytes of aging men (2), reaching 40% of leukocytes in individuals over 70 years (3). LOY increases over time and correlates with clonal expansion of myeloid cells (4). LOY also correlates with increased risk for mortality, cardiovascular events, and other age-associated disorders, but a causal relationship has not been established (2, 5). On page 292 of this issue, Sano et al. (6) determine that mLOY in myeloid cells is a major risk factor for increased incidence of cardiovascular and fibrotic diseases during aging.