Evidence map›Paper›PMID 40455700›Full record

ArticlePloS one2025

Mediating role of systemic inflammation in linking transferrin saturation to all-cause mortality in patients with coronary artery disease: Evidence from a large population-based study.

Zhenzhen Chen, Juan Guo, Haoying Chen, Yingying Guan, Simin Wang, Jianyu Zhou

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Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Zhenzhen ChenDepartment of Ultrasound, Taizhou Central Hospital, Taizhou, Zhejiang Province, China.
Juan GuoClinical Education Team, GE HealthCare Ultrasound, Wuhan, Hubei Province, China.ORCID 0000-0002-9302-5818
Haoying ChenDepartment of Ultrasound, Taizhou Central Hospital, Taizhou, Zhejiang Province, China.
Yingying GuanDepartment of Ultrasound, Taizhou Central Hospital, Taizhou, Zhejiang Province, China.
Simin WangDepartment of Ultrasound, Taizhou Central Hospital, Taizhou, Zhejiang Province, China.
Jianyu ZhouDepartment of Ultrasound, Taizhou Central Hospital, Taizhou, Zhejiang Province, China.ORCID 0009-0005-6747-9962

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTransferrin saturation (TS) is associated with mortality across populations, but its nonlinear relationship with all-cause mortality in coronary artery disease (CAD) and the role of systemic inflammation remain unclear. This study explored the association between TS and mortality in CAD patients, focusing on systemic inflammation as a potential mediator.

methodsData from National Health and Nutrition Examination Survey (NHANES) 1999-2006 included 769 CAD patients (>18 years) with available TS and mortality records. Systemic inflammation markers, such as the systemic immune-inflammation index (SII) and systemic inflammation response index (SIRI), were analyzed. Kaplan-Meier curves, Cox proportional hazards models, and mediation analyses examined the interactions between TS, inflammation, and mortality.

resultsA U-shaped relationship between TS and all-cause mortality was observed, with an inflection point at 30.5%. TS levels ≤30.5% were inversely associated with mortality (HR = 0.98; 95% CI, 0.96-0.99; P < 0.0001), while levels >30.5% increased mortality risk (HR = 1.05; 95% CI, 1.02-1.08; P < 0.001). Systemic inflammation markers (SII/SIRI) were associated with and may partially mediate the relationship between low TS (≤30.5%) and mortality. (mediation proportions: 28.5% and 21.8%, respectively). No mediation effects were found for TS > 30.5%.

conclusionsTS demonstrates a U-shaped relationship with all-cause mortality in CAD patients. Systemic inflammation is linked to both TS and mortality outcomes, suggesting potential mechanistic interplay. Maintaining TS within 20-30% and addressing inflammation may reduce mortality risk.

Indexed as

Coronary Artery DiseaseInflammationTransferrinAdultAgedBiomarkersFemaleHumansKaplan-Meier EstimateMaleMiddle AgedNutrition SurveysProportional Hazards ModelsRisk FactorsBiomarkersTransferrin

Identifiers

PMID40455700
PMCPMC12129200

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