Evidence map›Paper›PMID 41561117›Full record

ArticleFrontiers in cardiovascular medicine2025

Allostatic load-cardiovascular disease associations and the mediating effect of inflammatory factors: a prospective cohort study.

Shuai Xu, Ge Zhang, Yudi Xu, Chaoyang Yu, Ruhao Wu, Zhengrui Li, Teng Li, Xinyue Cui, Xufeng Huang, Shujing Zhou and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in cardiovascular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
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  3. Review
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

14 authors.

Shuai XuDepartment of Cardiology, The Fourth Affiliated Hospital of Soochow University, Suzhou Dushu Lake Hospital, Medical Center of Soochow University, Suzhou, China.
Ge ZhangDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Yudi XuDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Chaoyang YuDepartment of Vascular Surgery, First Hospital of Tsinghua University, Beijing, China.
Ruhao WuDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Zhengrui LiDepartment of Oral and Maxillofacial Head and Neck Oncology, Ninth People Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Teng LiDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Xinyue CuiDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Xufeng HuangFaculty of Medicine, University of Debrecen, Debrecen, Hungary.
Shujing ZhouFaculty of Medicine, University of Debrecen, Debrecen, Hungary.
Yahui HanSchool of Pharmacy, Harbin Medical University School of Pharmacy, Harbin, China.
Haonan ZhangDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Shiqian ZhangDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Yufeng JiangDepartment of Cardiology, The Fourth Affiliated Hospital of Soochow University, Suzhou Dushu Lake Hospital, Medical Center of Soochow University, Suzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Allostatic load (AL) captures multisystem dysregulation that accrues with chronic stress and may shape cardiovascular disease (CVD) risk through neuroendocrine and immune pathways. Robust population-scale evidence clarifying the exposure-response pattern and the extent of inflammatory mediation remains limited. Methods: In the UK Biobank, we analyzed 205,504 adults free of CVD at baseline from 502,366 recruited. An AL score was assembled from 12 routinely measured biomarkers. Incident CVD was ascertained via linkage to hospital and mortality records. We estimated adjusted hazard ratios (HRs) using Cox models and assessed nonlinearity with restricted cubic splines; robustness was evaluated in prespecified subgroups and sensitivity analyses. We also investigated the role of the mediating effect of inflammatory factors in the AL-CVD relationship. Results: Higher AL tracked with progressively greater CVD risk in a graded, non-linear pattern. Relative to AL = 0, AL> = 6 was associated with HR 2.15 (95% CI 1.99-2.33). Eight inflammatory markers met retention criteria for mediation; neutrophil count mediated 4.73% of the AL-CVD association. Group contrasts across AL tertiles indicated Cohen's d near 0.5 for several markers, largest for no-AL vs. high-AL. Conclusion: Elevated AL is linked to higher incident CVD with a non-linear exposure-response, and neutrophil-centric inflammation accounts for a measurable portion of the association. These findings support integrating stress-biology constructs and inflammatory profiling into cardiovascular risk assessment and prevention frameworks.

Indexed as

allostatic loadcardiovascular diseaseinflammatory factorsprospectiveUK Biobank

Identifiers

PMID41561117
PMCPMC12813168

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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.