Genome- and transcriptome-wide association meta-analysis reveals new insights into genes affecting coronary and peripheral artery disease
A low ankle-brachial Index (ABI) is an established condition for peripheral artery disease (PAD) and cardiovascular disease risk. The search for genetic determinants of the ankle-brachial index (ABI) is important to better understand molecular patho-cmechanisms of PAD and its commonalities with card...
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| Veröffentlicht in: | PloS one Jg. 20; H. 11; S. e0335513 |
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18.11.2025
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| Abstract | A low ankle-brachial Index (ABI) is an established condition for peripheral artery disease (PAD) and cardiovascular disease risk. The search for genetic determinants of the ankle-brachial index (ABI) is important to better understand molecular patho-cmechanisms of PAD and its commonalities with cardiovascular diseases (CVD), supporting development of new drug targets and tailored preventive or therapeutic measures.
To search for genetic factors contributing to ankle-brachial index, we integrated genome-wide association meta-analysis and transcriptome-wide association meta-analysis (TWAMA) of two German cohorts, the population-based LIFE-Adult cohort and LIFE-Heart, a cohort of patients with suspected or confirmed coronary artery disease. Pathway analysis of identified genes was used to explore biological mechanisms potentially involved in ABI pathophysiology. Finally, we analysed co-associations of known CAD or carotid plaque associations with ABI to detect possible genetic commonalities.
By our GWAS meta-analysis, we identified four new gene loci associated with ABI that are also linked with coronary artery diseases (CAD) (6q26: LPA and 11q14.1: DLG2) or cholesterol levels (12q21.31: TMTC2 and Xp21.1: DMD). Furthermore, we replicated a known ABI locus on cytoband 9p21.3 (CDKN2B) and four loci associated with PAD. In our TWAMA, we identified 145 blood transcripts associated with ABI at FDR 5% level. Gene set enrichment analysis of all TWAMA results revealed the inflammation-related pathways interferon gamma response, neutrophil degranulation, and interferon alpha response as the top three upregulated pathways in patients with lower ABI. Among overlapping genes between blood TWAMA and tissue-specific genetically regulated gene-expression association analysis, 24 genes showed consistent effect directions at nominal significance, with lower ABI-associated genes relating to stress response and vascular integrity, while higher ABI-associated genes linked to cellular homeostasis and metabolism.
In our integrated genome- and transcriptome-wide meta-analysis, we identified novel and confirmed known candidate genes and pathways associated with ABI. Association signals partly overlap with those of other cardiovascular traits such as CAD and carotid plaque formation. The integration of gene-expression data, validated known and added new molecular insight how inflammatory signalling can contribute to atherosclerosis and vascular dysfunction. These findings pave the way for improved understanding of the molecular underpinnings of PAD and inform future strategies for targeted prevention and therapy. |
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| AbstractList | A low ankle-brachial Index (ABI) is an established condition for peripheral artery disease (PAD) and cardiovascular disease risk. The search for genetic determinants of the ankle-brachial index (ABI) is important to better understand molecular patho-cmechanisms of PAD and its commonalities with cardiovascular diseases (CVD), supporting development of new drug targets and tailored preventive or therapeutic measures.
To search for genetic factors contributing to ankle-brachial index, we integrated genome-wide association meta-analysis and transcriptome-wide association meta-analysis (TWAMA) of two German cohorts, the population-based LIFE-Adult cohort and LIFE-Heart, a cohort of patients with suspected or confirmed coronary artery disease. Pathway analysis of identified genes was used to explore biological mechanisms potentially involved in ABI pathophysiology. Finally, we analysed co-associations of known CAD or carotid plaque associations with ABI to detect possible genetic commonalities.
By our GWAS meta-analysis, we identified four new gene loci associated with ABI that are also linked with coronary artery diseases (CAD) (6q26: LPA and 11q14.1: DLG2) or cholesterol levels (12q21.31: TMTC2 and Xp21.1: DMD). Furthermore, we replicated a known ABI locus on cytoband 9p21.3 (CDKN2B) and four loci associated with PAD. In our TWAMA, we identified 145 blood transcripts associated with ABI at FDR 5% level. Gene set enrichment analysis of all TWAMA results revealed the inflammation-related pathways interferon gamma response, neutrophil degranulation, and interferon alpha response as the top three upregulated pathways in patients with lower ABI. Among overlapping genes between blood TWAMA and tissue-specific genetically regulated gene-expression association analysis, 24 genes showed consistent effect directions at nominal significance, with lower ABI-associated genes relating to stress response and vascular integrity, while higher ABI-associated genes linked to cellular homeostasis and metabolism.
In our integrated genome- and transcriptome-wide meta-analysis, we identified novel and confirmed known candidate genes and pathways associated with ABI. Association signals partly overlap with those of other cardiovascular traits such as CAD and carotid plaque formation. The integration of gene-expression data, validated known and added new molecular insight how inflammatory signalling can contribute to atherosclerosis and vascular dysfunction. These findings pave the way for improved understanding of the molecular underpinnings of PAD and inform future strategies for targeted prevention and therapy. A low ankle-brachial Index (ABI) is an established condition for peripheral artery disease (PAD) and cardiovascular disease risk. The search for genetic determinants of the ankle-brachial index (ABI) is important to better understand molecular patho-cmechanisms of PAD and its commonalities with cardiovascular diseases (CVD), supporting development of new drug targets and tailored preventive or therapeutic measures. To search for genetic factors contributing to ankle-brachial index, we integrated genome-wide association meta-analysis and transcriptome-wide association meta-analysis (TWAMA) of two German cohorts, the population-based LIFE-Adult cohort and LIFE-Heart, a cohort of patients with suspected or confirmed coronary artery disease. Pathway analysis of identified genes was used to explore biological mechanisms potentially involved in ABI pathophysiology. Finally, we analysed co-associations of known CAD or carotid plaque associations with ABI to detect possible genetic commonalities. By our GWAS meta-analysis, we identified four new gene loci associated with ABI that are also linked with coronary artery diseases (CAD) (6q26: LPA and 11q14.1: DLG2) or cholesterol levels (12q21.31: TMTC2 and Xp21.1: DMD). Furthermore, we replicated a known ABI locus on cytoband 9p21.3 (CDKN2B) and four loci associated with PAD. In our TWAMA, we identified 145 blood transcripts associated with ABI at FDR 5% level. Gene set enrichment analysis of all TWAMA results revealed the inflammation-related pathways interferon gamma response, neutrophil degranulation, and interferon alpha response as the top three upregulated pathways in patients with lower ABI. Among overlapping genes between blood TWAMA and tissue-specific genetically regulated gene-expression association analysis, 24 genes showed consistent effect directions at nominal significance, with lower ABI-associated genes relating to stress response and vascular integrity, while higher ABI-associated genes linked to cellular homeostasis and metabolism. In our integrated genome- and transcriptome-wide meta-analysis, we identified novel and confirmed known candidate genes and pathways associated with ABI. Association signals partly overlap with those of other cardiovascular traits such as CAD and carotid plaque formation. The integration of gene-expression data, validated known and added new molecular insight how inflammatory signalling can contribute to atherosclerosis and vascular dysfunction. These findings pave the way for improved understanding of the molecular underpinnings of PAD and inform future strategies for targeted prevention and therapy. BackgroundA low ankle-brachial Index (ABI) is an established condition for peripheral artery disease (PAD) and cardiovascular disease risk. The search for genetic determinants of the ankle-brachial index (ABI) is important to better understand molecular patho-cmechanisms of PAD and its commonalities with cardiovascular diseases (CVD), supporting development of new drug targets and tailored preventive or therapeutic measures.MethodsTo search for genetic factors contributing to ankle-brachial index, we integrated genome-wide association meta-analysis and transcriptome-wide association meta-analysis (TWAMA) of two German cohorts, the population-based LIFE-Adult cohort and LIFE-Heart, a cohort of patients with suspected or confirmed coronary artery disease. Pathway analysis of identified genes was used to explore biological mechanisms potentially involved in ABI pathophysiology. Finally, we analysed co-associations of known CAD or carotid plaque associations with ABI to detect possible genetic commonalities.ResultsBy our GWAS meta-analysis, we identified four new gene loci associated with ABI that are also linked with coronary artery diseases (CAD) (6q26: LPA and 11q14.1: DLG2) or cholesterol levels (12q21.31: TMTC2 and Xp21.1: DMD). Furthermore, we replicated a known ABI locus on cytoband 9p21.3 (CDKN2B) and four loci associated with PAD. In our TWAMA, we identified 145 blood transcripts associated with ABI at FDR 5% level. Gene set enrichment analysis of all TWAMA results revealed the inflammation-related pathways interferon gamma response, neutrophil degranulation, and interferon alpha response as the top three upregulated pathways in patients with lower ABI. Among overlapping genes between blood TWAMA and tissue-specific genetically regulated gene-expression association analysis, 24 genes showed consistent effect directions at nominal significance, with lower ABI-associated genes relating to stress response and vascular integrity, while higher ABI-associated genes linked to cellular homeostasis and metabolism.ConclusionsIn our integrated genome- and transcriptome-wide meta-analysis, we identified novel and confirmed known candidate genes and pathways associated with ABI. Association signals partly overlap with those of other cardiovascular traits such as CAD and carotid plaque formation. The integration of gene-expression data, validated known and added new molecular insight how inflammatory signalling can contribute to atherosclerosis and vascular dysfunction. These findings pave the way for improved understanding of the molecular underpinnings of PAD and inform future strategies for targeted prevention and therapy. Background A low ankle-brachial Index (ABI) is an established condition for peripheral artery disease (PAD) and cardiovascular disease risk. The search for genetic determinants of the ankle-brachial index (ABI) is important to better understand molecular patho-cmechanisms of PAD and its commonalities with cardiovascular diseases (CVD), supporting development of new drug targets and tailored preventive or therapeutic measures. Methods To search for genetic factors contributing to ankle-brachial index, we integrated genome-wide association meta-analysis and transcriptome-wide association meta-analysis (TWAMA) of two German cohorts, the population-based LIFE-Adult cohort and LIFE-Heart, a cohort of patients with suspected or confirmed coronary artery disease. Pathway analysis of identified genes was used to explore biological mechanisms potentially involved in ABI pathophysiology. Finally, we analysed co-associations of known CAD or carotid plaque associations with ABI to detect possible genetic commonalities. Results By our GWAS meta-analysis, we identified four new gene loci associated with ABI that are also linked with coronary artery diseases (CAD) (6q26: LPA and 11q14.1: DLG2 ) or cholesterol levels (12q21.31: TMTC2 and Xp21.1: DMD ). Furthermore, we replicated a known ABI locus on cytoband 9p21.3 ( CDKN2B ) and four loci associated with PAD. In our TWAMA, we identified 145 blood transcripts associated with ABI at FDR 5% level. Gene set enrichment analysis of all TWAMA results revealed the inflammation-related pathways interferon gamma response , neutrophil degranulation , and interferon alpha response as the top three upregulated pathways in patients with lower ABI. Among overlapping genes between blood TWAMA and tissue-specific genetically regulated gene-expression association analysis, 24 genes showed consistent effect directions at nominal significance, with lower ABI-associated genes relating to stress response and vascular integrity, while higher ABI-associated genes linked to cellular homeostasis and metabolism. Conclusions In our integrated genome- and transcriptome-wide meta-analysis, we identified novel and confirmed known candidate genes and pathways associated with ABI. Association signals partly overlap with those of other cardiovascular traits such as CAD and carotid plaque formation. The integration of gene-expression data, validated known and added new molecular insight how inflammatory signalling can contribute to atherosclerosis and vascular dysfunction. These findings pave the way for improved understanding of the molecular underpinnings of PAD and inform future strategies for targeted prevention and therapy. Background A low ankle-brachial Index (ABI) is an established condition for peripheral artery disease (PAD) and cardiovascular disease risk. The search for genetic determinants of the ankle-brachial index (ABI) is important to better understand molecular patho-cmechanisms of PAD and its commonalities with cardiovascular diseases (CVD), supporting development of new drug targets and tailored preventive or therapeutic measures. Methods To search for genetic factors contributing to ankle-brachial index, we integrated genome-wide association meta-analysis and transcriptome-wide association meta-analysis (TWAMA) of two German cohorts, the population-based LIFE-Adult cohort and LIFE-Heart, a cohort of patients with suspected or confirmed coronary artery disease. Pathway analysis of identified genes was used to explore biological mechanisms potentially involved in ABI pathophysiology. Finally, we analysed co-associations of known CAD or carotid plaque associations with ABI to detect possible genetic commonalities. Results By our GWAS meta-analysis, we identified four new gene loci associated with ABI that are also linked with coronary artery diseases (CAD) (6q26: LPA and 11q14.1: DLG2) or cholesterol levels (12q21.31: TMTC2 and Xp21.1: DMD). Furthermore, we replicated a known ABI locus on cytoband 9p21.3 (CDKN2B) and four loci associated with PAD. In our TWAMA, we identified 145 blood transcripts associated with ABI at FDR 5% level. Gene set enrichment analysis of all TWAMA results revealed the inflammation-related pathways interferon gamma response, neutrophil degranulation, and interferon alpha response as the top three upregulated pathways in patients with lower ABI. Among overlapping genes between blood TWAMA and tissue-specific genetically regulated gene-expression association analysis, 24 genes showed consistent effect directions at nominal significance, with lower ABI-associated genes relating to stress response and vascular integrity, while higher ABI-associated genes linked to cellular homeostasis and metabolism. Conclusions In our integrated genome- and transcriptome-wide meta-analysis, we identified novel and confirmed known candidate genes and pathways associated with ABI. Association signals partly overlap with those of other cardiovascular traits such as CAD and carotid plaque formation. The integration of gene-expression data, validated known and added new molecular insight how inflammatory signalling can contribute to atherosclerosis and vascular dysfunction. These findings pave the way for improved understanding of the molecular underpinnings of PAD and inform future strategies for targeted prevention and therapy. A low ankle-brachial Index (ABI) is an established condition for peripheral artery disease (PAD) and cardiovascular disease risk. The search for genetic determinants of the ankle-brachial index (ABI) is important to better understand molecular patho-cmechanisms of PAD and its commonalities with cardiovascular diseases (CVD), supporting development of new drug targets and tailored preventive or therapeutic measures.BACKGROUNDA low ankle-brachial Index (ABI) is an established condition for peripheral artery disease (PAD) and cardiovascular disease risk. The search for genetic determinants of the ankle-brachial index (ABI) is important to better understand molecular patho-cmechanisms of PAD and its commonalities with cardiovascular diseases (CVD), supporting development of new drug targets and tailored preventive or therapeutic measures.To search for genetic factors contributing to ankle-brachial index, we integrated genome-wide association meta-analysis and transcriptome-wide association meta-analysis (TWAMA) of two German cohorts, the population-based LIFE-Adult cohort and LIFE-Heart, a cohort of patients with suspected or confirmed coronary artery disease. Pathway analysis of identified genes was used to explore biological mechanisms potentially involved in ABI pathophysiology. Finally, we analysed co-associations of known CAD or carotid plaque associations with ABI to detect possible genetic commonalities.METHODSTo search for genetic factors contributing to ankle-brachial index, we integrated genome-wide association meta-analysis and transcriptome-wide association meta-analysis (TWAMA) of two German cohorts, the population-based LIFE-Adult cohort and LIFE-Heart, a cohort of patients with suspected or confirmed coronary artery disease. Pathway analysis of identified genes was used to explore biological mechanisms potentially involved in ABI pathophysiology. Finally, we analysed co-associations of known CAD or carotid plaque associations with ABI to detect possible genetic commonalities.By our GWAS meta-analysis, we identified four new gene loci associated with ABI that are also linked with coronary artery diseases (CAD) (6q26: LPA and 11q14.1: DLG2) or cholesterol levels (12q21.31: TMTC2 and Xp21.1: DMD). Furthermore, we replicated a known ABI locus on cytoband 9p21.3 (CDKN2B) and four loci associated with PAD. In our TWAMA, we identified 145 blood transcripts associated with ABI at FDR 5% level. Gene set enrichment analysis of all TWAMA results revealed the inflammation-related pathways interferon gamma response, neutrophil degranulation, and interferon alpha response as the top three upregulated pathways in patients with lower ABI. Among overlapping genes between blood TWAMA and tissue-specific genetically regulated gene-expression association analysis, 24 genes showed consistent effect directions at nominal significance, with lower ABI-associated genes relating to stress response and vascular integrity, while higher ABI-associated genes linked to cellular homeostasis and metabolism.RESULTSBy our GWAS meta-analysis, we identified four new gene loci associated with ABI that are also linked with coronary artery diseases (CAD) (6q26: LPA and 11q14.1: DLG2) or cholesterol levels (12q21.31: TMTC2 and Xp21.1: DMD). Furthermore, we replicated a known ABI locus on cytoband 9p21.3 (CDKN2B) and four loci associated with PAD. In our TWAMA, we identified 145 blood transcripts associated with ABI at FDR 5% level. Gene set enrichment analysis of all TWAMA results revealed the inflammation-related pathways interferon gamma response, neutrophil degranulation, and interferon alpha response as the top three upregulated pathways in patients with lower ABI. Among overlapping genes between blood TWAMA and tissue-specific genetically regulated gene-expression association analysis, 24 genes showed consistent effect directions at nominal significance, with lower ABI-associated genes relating to stress response and vascular integrity, while higher ABI-associated genes linked to cellular homeostasis and metabolism.In our integrated genome- and transcriptome-wide meta-analysis, we identified novel and confirmed known candidate genes and pathways associated with ABI. Association signals partly overlap with those of other cardiovascular traits such as CAD and carotid plaque formation. The integration of gene-expression data, validated known and added new molecular insight how inflammatory signalling can contribute to atherosclerosis and vascular dysfunction. These findings pave the way for improved understanding of the molecular underpinnings of PAD and inform future strategies for targeted prevention and therapy.CONCLUSIONSIn our integrated genome- and transcriptome-wide meta-analysis, we identified novel and confirmed known candidate genes and pathways associated with ABI. Association signals partly overlap with those of other cardiovascular traits such as CAD and carotid plaque formation. The integration of gene-expression data, validated known and added new molecular insight how inflammatory signalling can contribute to atherosclerosis and vascular dysfunction. These findings pave the way for improved understanding of the molecular underpinnings of PAD and inform future strategies for targeted prevention and therapy. |
| Audience | Academic |
| Author | Horn, Katrin Rode, Michael Pott, Janne Wirkner, Kerstin Thiery, Joachim Henger, Sylvia Scholz, Markus Teren, Andrej Kirsten, Holger Rosolowski, Maciej Loeffler, Markus |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/41252360$$D View this record in MEDLINE/PubMed |
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| Copyright | Copyright: © 2025 Rode et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. COPYRIGHT 2025 Public Library of Science 2025 Rode et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2025 Rode et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| DOI | 10.1371/journal.pone.0335513 |
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| Snippet | A low ankle-brachial Index (ABI) is an established condition for peripheral artery disease (PAD) and cardiovascular disease risk. The search for genetic... Background A low ankle-brachial Index (ABI) is an established condition for peripheral artery disease (PAD) and cardiovascular disease risk. The search for... BackgroundA low ankle-brachial Index (ABI) is an established condition for peripheral artery disease (PAD) and cardiovascular disease risk. The search for... Background A low ankle-brachial Index (ABI) is an established condition for peripheral artery disease (PAD) and cardiovascular disease risk. The search for... |
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| SubjectTerms | Aged Analysis Ankle Ankle Brachial Index Arteriosclerosis Association analysis Atherosclerosis Blood Blood pressure Calcification Cardiovascular disease Cardiovascular diseases Cellular stress response Cholesterol Chronic illnesses Coronary artery disease Coronary Artery Disease - genetics Coronary heart disease Coronary vessels Data collection Degranulation Dystrophin Female Gene expression Gene set enrichment analysis Genes Genetic factors Genetic Predisposition to Disease Genome-Wide Association Study Genomes Genomic analysis Genomics Health aspects Health risks Heart attacks Heart diseases Homeostasis Humans Interferon Leukocytes (neutrophilic) Male Measurement Meta-analysis Middle Aged Mortality Pathophysiology Peripheral Arterial Disease - genetics Polymorphism, Single Nucleotide Quality control Signal transduction Therapeutic targets Transcriptome Transcriptomes Vascular diseases Vein & artery diseases |
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| Title | Genome- and transcriptome-wide association meta-analysis reveals new insights into genes affecting coronary and peripheral artery disease |
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