Epigenome-wide DNA methylation association study of CHIP provides insight into perturbed gene regulation

With age, hematopoietic stem cells can acquire somatic mutations in leukemogenic genes that confer a proliferative advantage in a phenomenon termed CHIP. How these mutations result in increased risk for numerous age-related diseases remains poorly understood. We conduct a multiracial meta-analysis o...

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Vydáno v:Nature communications Ročník 16; číslo 1; s. 4678 - 14
Hlavní autoři: Kirmani, Sara, Huan, Tianxiao, Van Amburg, Joseph C., Joehanes, Roby, Uddin, Md Mesbah, Nguyen, Ngoc Quynh H., Yu, Bing, Brody, Jennifer A., Fornage, Myriam, Bressler, Jan, Sotoodehnia, Nona, Ong, David A., Puddu, Fabio, Floyd, James S., Ballantyne, Christie M., Psaty, Bruce M., Raffield, Laura M., Natarajan, Pradeep, Conneely, Karen N., Weinstock, Joshua S., Carson, April P., Lange, Leslie A., Ferrier, Kendra, Heard-Costa, Nancy L., Murabito, Joanne, Bick, Alexander G., Levy, Daniel
Médium: Journal Article
Jazyk:angličtina
Vydáno: London Nature Publishing Group UK 20.05.2025
Nature Publishing Group
Nature Portfolio
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13/100
13/31
38/91
45/22
45/23
45/41
631/208/176/1988
631/208/457
631/250/232
631/443/592/75
631/443/7
Age
Age related diseases
Aged
Arteriosclerosis
Atherosclerosis
Atherosclerosis - genetics
Blood cells
Cardiovascular diseases
Cardiovascular Diseases - genetics
Cardiovascular Diseases - mortality
Cell culture
CpG Islands - genetics
DNA methylation
DNA Methylation - genetics
Epigenesis, Genetic
Epigenetics
Epigenome - genetics
Female
Gene Expression Regulation
Gene regulation
Genome-Wide Association Study
Health risks
Hematopoietic stem cells
Hematopoietic Stem Cells - metabolism
Humanities and Social Sciences
Humans
Male
Middle Aged
Molecular modelling
multidisciplinary
Mutation
Risk
Science
Science (multidisciplinary)
Stem cells
Transcriptomics
ISSN:2041-1723, 2041-1723
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Abstract With age, hematopoietic stem cells can acquire somatic mutations in leukemogenic genes that confer a proliferative advantage in a phenomenon termed CHIP. How these mutations result in increased risk for numerous age-related diseases remains poorly understood. We conduct a multiracial meta-analysis of EWAS of CHIP in the Framingham Heart Study, Jackson Heart Study, Cardiovascular Health Study, and Atherosclerosis Risk in Communities cohorts ( N  = 8196) to elucidate the molecular mechanisms underlying CHIP and illuminate how these changes influence cardiovascular disease risk. We functionally validate the EWAS findings using human hematopoietic stem cell models of CHIP. We then use expression quantitative trait methylation analysis to identify transcriptomic changes associated with CHIP-associated CpGs. Causal inference analyses reveal 261 CHIP-associated CpGs associated with cardiovascular traits and all-cause mortality (FDR adjusted p -value < 0.05). Taken together, our study reports the epigenetic changes impacted by CHIP and their associations with age-related disease outcomes. In CHIP, somatic mutations in a hematopoietic stem cell lead to a clonal subpopulation of blood cells. Here, the authors perform a CHIP meta-EWAS to establish its epigenetic features and age-related outcomes.
AbstractList With age, hematopoietic stem cells can acquire somatic mutations in leukemogenic genes that confer a proliferative advantage in a phenomenon termed CHIP. How these mutations result in increased risk for numerous age-related diseases remains poorly understood. We conduct a multiracial meta-analysis of EWAS of CHIP in the Framingham Heart Study, Jackson Heart Study, Cardiovascular Health Study, and Atherosclerosis Risk in Communities cohorts (N = 8196) to elucidate the molecular mechanisms underlying CHIP and illuminate how these changes influence cardiovascular disease risk. We functionally validate the EWAS findings using human hematopoietic stem cell models of CHIP. We then use expression quantitative trait methylation analysis to identify transcriptomic changes associated with CHIP-associated CpGs. Causal inference analyses reveal 261 CHIP-associated CpGs associated with cardiovascular traits and all-cause mortality (FDR adjusted p-value < 0.05). Taken together, our study reports the epigenetic changes impacted by CHIP and their associations with age-related disease outcomes. In CHIP, somatic mutations in a hematopoietic stem cell lead to a clonal subpopulation of blood cells. Here, the authors perform a CHIP meta-EWAS to establish its epigenetic features and age-related outcomes.
With age, hematopoietic stem cells can acquire somatic mutations in leukemogenic genes that confer a proliferative advantage in a phenomenon termed CHIP. How these mutations result in increased risk for numerous age-related diseases remains poorly understood. We conduct a multiracial meta-analysis of EWAS of CHIP in the Framingham Heart Study, Jackson Heart Study, Cardiovascular Health Study, and Atherosclerosis Risk in Communities cohorts (N = 8196) to elucidate the molecular mechanisms underlying CHIP and illuminate how these changes influence cardiovascular disease risk. We functionally validate the EWAS findings using human hematopoietic stem cell models of CHIP. We then use expression quantitative trait methylation analysis to identify transcriptomic changes associated with CHIP-associated CpGs. Causal inference analyses reveal 261 CHIP-associated CpGs associated with cardiovascular traits and all-cause mortality (FDR adjusted p-value < 0.05). Taken together, our study reports the epigenetic changes impacted by CHIP and their associations with age-related disease outcomes.With age, hematopoietic stem cells can acquire somatic mutations in leukemogenic genes that confer a proliferative advantage in a phenomenon termed CHIP. How these mutations result in increased risk for numerous age-related diseases remains poorly understood. We conduct a multiracial meta-analysis of EWAS of CHIP in the Framingham Heart Study, Jackson Heart Study, Cardiovascular Health Study, and Atherosclerosis Risk in Communities cohorts (N = 8196) to elucidate the molecular mechanisms underlying CHIP and illuminate how these changes influence cardiovascular disease risk. We functionally validate the EWAS findings using human hematopoietic stem cell models of CHIP. We then use expression quantitative trait methylation analysis to identify transcriptomic changes associated with CHIP-associated CpGs. Causal inference analyses reveal 261 CHIP-associated CpGs associated with cardiovascular traits and all-cause mortality (FDR adjusted p-value < 0.05). Taken together, our study reports the epigenetic changes impacted by CHIP and their associations with age-related disease outcomes.
With age, hematopoietic stem cells can acquire somatic mutations in leukemogenic genes that confer a proliferative advantage in a phenomenon termed CHIP. How these mutations result in increased risk for numerous age-related diseases remains poorly understood. We conduct a multiracial meta-analysis of EWAS of CHIP in the Framingham Heart Study, Jackson Heart Study, Cardiovascular Health Study, and Atherosclerosis Risk in Communities cohorts ( N = 8196) to elucidate the molecular mechanisms underlying CHIP and illuminate how these changes influence cardiovascular disease risk. We functionally validate the EWAS findings using human hematopoietic stem cell models of CHIP. We then use expression quantitative trait methylation analysis to identify transcriptomic changes associated with CHIP-associated CpGs. Causal inference analyses reveal 261 CHIP-associated CpGs associated with cardiovascular traits and all-cause mortality (FDR adjusted p -value < 0.05). Taken together, our study reports the epigenetic changes impacted by CHIP and their associations with age-related disease outcomes.
Abstract With age, hematopoietic stem cells can acquire somatic mutations in leukemogenic genes that confer a proliferative advantage in a phenomenon termed CHIP. How these mutations result in increased risk for numerous age-related diseases remains poorly understood. We conduct a multiracial meta-analysis of EWAS of CHIP in the Framingham Heart Study, Jackson Heart Study, Cardiovascular Health Study, and Atherosclerosis Risk in Communities cohorts (N = 8196) to elucidate the molecular mechanisms underlying CHIP and illuminate how these changes influence cardiovascular disease risk. We functionally validate the EWAS findings using human hematopoietic stem cell models of CHIP. We then use expression quantitative trait methylation analysis to identify transcriptomic changes associated with CHIP-associated CpGs. Causal inference analyses reveal 261 CHIP-associated CpGs associated with cardiovascular traits and all-cause mortality (FDR adjusted p-value < 0.05). Taken together, our study reports the epigenetic changes impacted by CHIP and their associations with age-related disease outcomes.
With age, hematopoietic stem cells can acquire somatic mutations in leukemogenic genes that confer a proliferative advantage in a phenomenon termed CHIP. How these mutations result in increased risk for numerous age-related diseases remains poorly understood. We conduct a multiracial meta-analysis of EWAS of CHIP in the Framingham Heart Study, Jackson Heart Study, Cardiovascular Health Study, and Atherosclerosis Risk in Communities cohorts ( N  = 8196) to elucidate the molecular mechanisms underlying CHIP and illuminate how these changes influence cardiovascular disease risk. We functionally validate the EWAS findings using human hematopoietic stem cell models of CHIP. We then use expression quantitative trait methylation analysis to identify transcriptomic changes associated with CHIP-associated CpGs. Causal inference analyses reveal 261 CHIP-associated CpGs associated with cardiovascular traits and all-cause mortality (FDR adjusted p -value < 0.05). Taken together, our study reports the epigenetic changes impacted by CHIP and their associations with age-related disease outcomes. In CHIP, somatic mutations in a hematopoietic stem cell lead to a clonal subpopulation of blood cells. Here, the authors perform a CHIP meta-EWAS to establish its epigenetic features and age-related outcomes.
ArticleNumber 4678
Author Ballantyne, Christie M.
Ong, David A.
Ferrier, Kendra
Psaty, Bruce M.
Natarajan, Pradeep
Huan, Tianxiao
Floyd, James S.
Nguyen, Ngoc Quynh H.
Sotoodehnia, Nona
Bick, Alexander G.
Fornage, Myriam
Raffield, Laura M.
Uddin, Md Mesbah
Conneely, Karen N.
Heard-Costa, Nancy L.
Brody, Jennifer A.
Joehanes, Roby
Weinstock, Joshua S.
Murabito, Joanne
Yu, Bing
Lange, Leslie A.
Kirmani, Sara
Bressler, Jan
Van Amburg, Joseph C.
Levy, Daniel
Puddu, Fabio
Carson, April P.
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/40393957$$D View this record in MEDLINE/PubMed
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Snippet With age, hematopoietic stem cells can acquire somatic mutations in leukemogenic genes that confer a proliferative advantage in a phenomenon termed CHIP. How...
Abstract With age, hematopoietic stem cells can acquire somatic mutations in leukemogenic genes that confer a proliferative advantage in a phenomenon termed...
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Atherosclerosis
Atherosclerosis - genetics
Blood cells
Cardiovascular diseases
Cardiovascular Diseases - genetics
Cardiovascular Diseases - mortality
Cell culture
CpG Islands - genetics
DNA methylation
DNA Methylation - genetics
Epigenesis, Genetic
Epigenetics
Epigenome - genetics
Female
Gene Expression Regulation
Gene regulation
Genome-Wide Association Study
Health risks
Hematopoietic stem cells
Hematopoietic Stem Cells - metabolism
Humanities and Social Sciences
Humans
Male
Middle Aged
Molecular modelling
multidisciplinary
Mutation
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Science
Science (multidisciplinary)
Stem cells
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Title Epigenome-wide DNA methylation association study of CHIP provides insight into perturbed gene regulation
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