Evidence map›Paper›PMID 42404310›Full record

ArticleThe journal of cardiovascular aging2025

Age-related cardiovascular disease and mosaic hematopoietic loss of the Y chromosome.

Nicholas W Chavkin

Abstract read
In one paragraph

Article in The journal of cardiovascular aging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Nicholas W ChavkinCenter for Developmental Biology and Regenerative Medicine, Seattle Children's Research Institute, Seattle, WA 98101, USA.ORCID 0000-0001-9058-0245

Funding

The Role of Hematopoietic Loss of Y Chromosome on Aging PhenotypesK22AG081323 · NIA · SEATTLE CHILDREN'S HOSPITAL · PI Nicholas W Chavkin · 2024 to 2026
$559k
American Heart Association-American Stroke Association 23CDA1054358NIA NIH HHS K22 AG081323
6 · The paper itself

Abstract

Age is the strongest risk factor for cardiovascular morbidity and mortality, driven in part by aging leukocytes negatively impact cardiovascular health. This effect is particularly pronounced in men, who have a shorter average lifespan-approximately six years less than women, largely due to higher mortality rates in old age. One contributing factor is a male-specific aging blood phenotype characterized by the mosaic loss of the Y chromosome (mLOY), a condition in which a subset of blood cells lose the Y chromosome. mLOY is highly prevalent in elderly men, affecting 45% of those aged 70 and older. Recent studies have linked mLOY to increased early mortality, age-related pathologies, and cardiovascular disease, potentially explaining the observed sex discrepancy in life expectancy. Experimental studies have begun to uncover potential mechanisms related to leukocyte responses to cardiac injury and the polarization of macrophages that promote pro-fibrotic cytokine expression. Current evidence suggests that mLOY reflects an underlying aspect of biological aging related to genomic instability, which drives age-related diseases, including cardiovascular conditions. Although mLOY shares similarities with general age-related changes in the hematopoietic system, it may exert distinct effects on leukocytes that promote cardiovascular disease through enhanced tissue fibrosis pathways. These findings highlight that mLOY accumulates with age and contributes to cardiovascular disease through mechanisms that are independent of biological aging per se. Further investigation into mLOY-specific pathways in aging and age-related diseases may reveal novel therapeutic targets for a chronic condition that affects a large proportion of the elderly male population. This review discusses the current literature on mLOY and its connection to cardiovascular disease within the broader context of aging.

Indexed as

age-related cardiovascular diseaseclonal hematopoiesismosaic chromosomal alterationsmosaic Loss of Y chromosomeSex chromosome aneuploidy

Identifiers

PMID42404310
PMCPMC13330738

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.