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@ARTICLE{Wielscher:179780,
author = {M. Wielscher and P. R. Mandaviya and B. Kuehnel and R.
Joehanes and R. Mustafa and O. Robinson and Y. Zhang$^*$ and
B. Bodinier and E. Walton and P. P. Mishra and P. Schlosser
and R. Wilson and P.-C. Tsai and S. Palaniswamy and R. E.
Marioni and G. Fiorito and G. Cugliari and V. Karhunen and
M. Ghanbari and B. M. Psaty and M. Loh and J. C. Bis and B.
Lehne and N. Sotoodehnia and I. J. Deary and M. Chadeau-Hyam
and J. A. Brody and A. Cardona and E. Selvin and A. K. Smith
and A. H. Miller and M. A. Torres and E. Marouli and X.
Gao$^*$ and J. B. J. van Meurs and J. Graf-Schindler and W.
Rathmann and W. Koenig and A. Peters and W. Weninger and M.
Farlik and T. Zhang and W. Chen and Y. Xia and A. Teumer and
M. Nauck and H. J. Grabe and M. Doerr and T. Lehtimäki and
W. Guan and L. Milani and T. Tanaka and K. Fisher and L. L.
Waite and S. Kasela and P. Vineis and N. Verweij and P. van
der Harst and L. Iacoviello and C. Sacerdote and S. Panico
and V. Krogh and R. Tumino and E. Tzala and G. Matullo and
M. A. Hurme and O. T. Raitakari and E. Colicino and A. A.
Baccarelli and M. Kähönen and K.-H. Herzig and S. Li and
K. N. Conneely and J. S. Kooner and A. Köttgen and B. T.
Heijmans and P. Deloukas and C. Relton and K. K. Ong and J.
T. Bell and E. Boerwinkle and P. Elliott and H. Brenner$^*$
and M. Beekman and D. Levy and M. Waldenberger and J. C.
Chambers and A. Dehghan and M.-R. Järvelin},
collaboration = {B. consortium},
title = {{DNA} methylation signature of chronic low-grade
inflammation and its role in cardio-respiratory diseases.},
journal = {Nature Communications},
volume = {13},
number = {1},
issn = {2041-1723},
address = {[London]},
publisher = {Nature Publishing Group UK},
reportid = {DKFZ-2022-00887},
pages = {2408},
year = {2022},
abstract = {We performed a multi-ethnic Epigenome Wide Association
study on 22,774 individuals to describe the DNA methylation
signature of chronic low-grade inflammation as measured by
C-Reactive protein (CRP). We find 1,511 independent
differentially methylated loci associated with CRP. These
CpG sites show correlation structures across chromosomes,
and are primarily situated in euchromatin, depleted in CpG
islands. These genomic loci are predominantly situated in
transcription factor binding sites and genomic enhancer
regions. Mendelian randomization analysis suggests altered
CpG methylation is a consequence of increased blood CRP
levels. Mediation analysis reveals obesity and smoking as
important underlying driving factors for changed CpG
methylation. Finally, we find that an activated CpG
signature significantly increases the risk for
cardiometabolic diseases and COPD.},
cin = {C070},
ddc = {500},
cid = {I:(DE-He78)C070-20160331},
pnm = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
pid = {G:(DE-HGF)POF4-313},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:35504910},
doi = {10.1038/s41467-022-29792-6},
url = {https://inrepo02.dkfz.de/record/179780},
}