NDLI: Iron and hepcidin as risk factors in atherosclerosis: what do the genes say?

Content Provider	Springer Nature : BioMed Central
Author	Galesloot, Tessel E. Janss, Luc L. Burgess, Stephen Kiemeney, Lambertus A. L. M. den Heijer, Martin de Graaf, Jacqueline Holewijn, Suzanne Benyamin, Beben Whitfield, John B. Swinkels, Dorine W. Vermeulen, Sita H.
Abstract	Background Previous reports suggested a role for iron and hepcidin in atherosclerosis. Here, we evaluated the causality of these associations from a genetic perspective via (i) a Mendelian randomization (MR) approach, (ii) study of association of atherosclerosis-related single nucleotide polymorphisms (SNPs) with iron and hepcidin, and (iii) estimation of genomic correlations between hepcidin, iron and atherosclerosis. Results Analyses were performed in a general population sample. Iron parameters (serum iron, serum ferritin, total iron-binding capacity and transferrin saturation), serum hepcidin and genome-wide SNP data were available for N = 1,819; non-invasive measurements of atherosclerosis (NIMA), i.e., presence of plaque, intima media thickness and ankle-brachial index (ABI), for N = 549. For the MR, we used 12 iron-related SNPs that were previously identified in a genome-wide association meta-analysis on iron status, and assessed associations of individual SNPs and quartiles of a multi-SNP score with NIMA. Quartile 4 versus quartile 1 of the multi-SNP score showed directionally consistent associations with the hypothesized direction of effect for all NIMA in women, indicating that increased body iron status is a risk factor for atherosclerosis in women. We observed no single SNP associations that fit the hypothesized directions of effect between iron and NIMA, except for rs651007, associated with decreased ferritin concentration and decreased atherosclerosis risk. Two of six NIMA-related SNPs showed association with the ratio hepcidin/ferritin, suggesting that an increased hepcidin/ferritin ratio increases atherosclerosis risk. Genomic correlations were close to zero, except for hepcidin and ferritin with ABI at rest [−0.27 (SE 0.34) and −0.22 (SE 0.35), respectively] and ABI after exercise [−0.29 (SE 0.34) and −0.30 (0.35), respectively]. The negative sign indicates an increased atherosclerosis risk with increased hepcidin and ferritin concentrations. Conclusions Our results suggest a potential causal role for hepcidin and ferritin in atherosclerosis, and may indicate that iron status is causally related to atherosclerosis in women.
Related Links	https://bmcgenomdata.biomedcentral.com/counter/pdf/10.1186/s12863-015-0246-4.pdf
Ending Page	12
Page Count	12
Starting Page	1
File Format	HTM / HTML
ISSN	27306844
DOI	10.1186/s12863-015-0246-4
Journal	BMC Genomic Data
Issue Number	1
Volume Number	16
Language	English
Publisher	BioMed Central
Publisher Date	2015-07-11
Access Restriction	Open
Subject Keyword	Life Sciences Animal Genetics and Genomics Microbial Genetics and Genomics Plant Genetics and Genomics Genetics and Population Dynamics Hepcidin Iron Atherosclerosis Cardiovascular disease General population Mendelian randomization
Content Type	Text
Resource Type	Article
Subject	Health Informatics Genetics
Journal Impact Factor	1.9/2023
5-Year Journal Impact Factor	1.9/2023

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Iron and hepcidin as risk factors in atherosclerosis: what do the genes say?

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