@article {9181,
	title = {{Clonal hematopoiesis of indeterminate potential, DNA methylation, and risk for coronary artery disease},
	journal = {Nat Commun},
	volume = {13},
	year = {2022},
	month = {Sep},
	pages = {5350},
	abstract = {Age-related changes to the genome-wide DNA methylation (DNAm) pattern observed in blood are well-documented. Clonal hematopoiesis of indeterminate potential (CHIP), characterized by the age-related acquisition and expansion of leukemogenic mutations in hematopoietic stem cells (HSCs), is associated with blood cancer and coronary artery disease (CAD). Epigenetic regulators DNMT3A and TET2 are the two most frequently mutated CHIP genes. Here, we present results from an epigenome-wide association study for CHIP in 582 Cardiovascular Health Study (CHS) participants, with replication in 2655 Atherosclerosis Risk in Communities (ARIC) Study participants. We show that DNMT3A and TET2 CHIP have distinct and directionally opposing genome-wide DNAm association patterns consistent with their regulatory roles, albeit both promoting self-renewal of HSCs. Mendelian randomization analyses indicate that a subset of DNAm alterations associated with these two leading CHIP genes may promote the risk for CAD.},
	author = {Uddin, M. D. M. and Nguyen, N. Q. H. and Yu, B. and Brody, J. A. and Pampana, A. and Nakao, T. and Fornage, M. and Bressler, J. and Sotoodehnia, N. and Weinstock, J. S. and Honigberg, M. C. and Nachun, D. and Bhattacharya, R. and Griffin, G. K. and Chander, V. and Gibbs, R. A. and Rotter, J. I. and Liu, C. and Baccarelli, A. A. and Chasman, D. I. and Whitsel, E. A. and Kiel, D. P. and Murabito, J. M. and Boerwinkle, E. and Ebert, B. L. and Jaiswal, S. and Floyd, J. S. and Bick, A. G. and Ballantyne, C. M. and Psaty, B. M. and Natarajan, P. and Conneely, K. N.}
}
@article {9111,
	title = {{DNA methylation signature of chronic low-grade inflammation and its role in cardio-respiratory diseases},
	journal = {Nat Commun},
	volume = {13},
	year = {2022},
	month = {05},
	pages = {2408},
	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.},
	author = {Wielscher, M. and Mandaviya, P. R. and Kuehnel, B. and Joehanes, R. and Mustafa, R. and Robinson, O. and Zhang, Y. and Bodinier, B. and Walton, E. and Mishra, P. P. and Schlosser, P. and Wilson, R. and Tsai, P. C. and Palaniswamy, S. and Marioni, R. E. and Fiorito, G. and Cugliari, G. and Karhunen, V. and Ghanbari, M. and Psaty, B. M. and Loh, M. and Bis, J. C. and Lehne, B. and Sotoodehnia, N. and Deary, I. J. and Chadeau-Hyam, M. and Brody, J. A. and Cardona, A. and Selvin, E. and Smith, A. K. and Miller, A. H. and Torres, M. A. and Marouli, E. and G{\`a}o, X. and van Meurs, J. B. J. and Graf-Schindler, J. and Rathmann, W. and Koenig, W. and Peters, A. and Weninger, W. and Farlik, M. and Zhang, T. and Chen, W. and Xia, Y. and Teumer, A. and Nauck, M. and Grabe, H. J. and Doerr, M. and Lehtim{\"a}ki, T. and Guan, W. and Milani, L. and Tanaka, T. and Fisher, K. and Waite, L. L. and Kasela, S. and Vineis, P. and Verweij, N. and van der Harst, P. and Iacoviello, L. and Sacerdote, C. and Panico, S. and Krogh, V. and Tumino, R. and Tzala, E. and Matullo, G. and Hurme, M. A. and Raitakari, O. T. and Colicino, E. and Baccarelli, A. A. and K{\"a}h{\"o}nen, M. and Herzig, K. H. and Li, S. and Conneely, K. N. and Kooner, J. S. and K{\"o}ttgen, A. and Heijmans, B. T. and Deloukas, P. and Relton, C. and Ong, K. K. and Bell, J. T. and Boerwinkle, E. and Elliott, P. and Brenner, H. and Beekman, M. and Levy, D. and Waldenberger, M. and Chambers, J. C. and Dehghan, A. and Jarvelin, M. R.}
}
