Evidence map›Paper›PMID 39159130›Full record

ArticleAging2024

DNA methylation-estimated phenotypes, telomere length and risk of ischemic stroke: epigenetic age acceleration of screening and a Mendelian randomization study.

Aierpati Maimaiti, Jianhua Ma, Chenguang Hao, Dengfeng Han, Yongxin Wang, Zengliang Wang, Rena Abudusalamu

Abstract read
In one paragraph

Article in Aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
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

7 authors.

Aierpati MaimaitiDepartment of Neurosurgery, Neurosurgery Centre, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang 830054, China.
Jianhua MaDepartment of Neurology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang 830054, China.
Chenguang HaoDepartment of Neurology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang 830054, China.
Dengfeng HanDepartment of Neurology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang 830054, China.
Yongxin WangDepartment of Neurosurgery, Neurosurgery Centre, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang 830054, China.
Zengliang WangDepartment of Neurosurgery, Neurosurgery Centre, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang 830054, China.
Rena AbudusalamuDepartment of Neurology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang 830054, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAging is a complex biological process that may be accelerated in certain pathological conditions. DNA methylation age (DNAmAge) has emerged as a biomarker for biological age, which can differ from chronological age. This research peels back the layers of the relationship between fast-forward aging and ischemic stroke, poking and prodding the potential two-way causal influences between stroke and biological aging indicators.

methodsWe analyzed a cohort of ischemic stroke patients, comparing DNAmAge with chronological age to measure age acceleration. We assessed variations in age acceleration among stroke subtypes and between sexes. Using Mendelian randomization, we examined the causal links between stroke, aging biomarkers like telomere length, and age acceleration's effect on stroke risk.

resultsOur investigation reveals a pronounced association between ischemic stroke and age acceleration, most notably in patients with cardioembolic strokes, who exhibited a striking median difference of 9 years between DNAmAge and chronological age. Furthermore, age acceleration differed significantly across stroke subtypes and was higher in women than in men. In terms of causality, MR analysis indicated a modest negative effect of stroke on telomere length, but no causal effect of age phenotypes on stroke or its subtypes. However, some indication of a potential causal effect of ischemic stroke on PhenoAge acceleration was observed.

conclusionThe study provides insight into the relationship between DNAmAge and ischemic stroke, particularly cardioembolic stroke, and suggests possible gender differences. These insights carry profound clinical significance and set stage for future investigations into the entwined pathways of stroke and accelerated aging.

Indexed as

AgingDNA MethylationEpigenesis, GeneticIschemic StrokeMendelian Randomization AnalysisPhenotypeAgedFemaleHumansMaleMiddle AgedRisk FactorsTelomereTelomere Homeostasisepigenetic age accelerationischemic strokemendelian randomizationmethylation clockstroke subtypes

Identifiers

PMID39159130
PMCPMC11386914

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.