. 2025 Mar 21;17(1):27.

doi: 10.1186/s13073-025-01456-2.

Rare damaging CCR2 variants are associated with lower lifetime cardiovascular risk

Marios K Georgakis^#^{1

2

3}, Rainer Malik^#⁴, Omar El Bounkari⁴, Natalie R Hasbani⁵, Jiang Li⁶, Jennifer E Huffman⁷, Gabrielle Shakt^{8

9}, Reinier W P Tack^{10

11}, Tamara N Kimball^{10

12}, Yaw Asare⁴, Alanna C Morrison⁵, Noah L Tsao^{8

9}, Renae Judy^{8

9}, Braxton D Mitchell^{13

14}, Huichun Xu¹³, May E Montasser¹³, Ron Do^{15

16}, Eimear E Kenny^{15

17

18

19}, Ruth J F Loos¹⁵, James G Terry²⁰, John Jeffrey Carr²⁰, Joshua C Bis²¹, Bruce M Psaty^{21

22

23}, W T Longstreth^{23

24}, Kendra A Young²⁵, Sharon M Lutz^{26

27}, Michael H Cho²⁸, Jai Broome²⁹, Alyna T Khan²⁹, Fei Fei Wang²⁹, Nancy Heard-Costa^{30

31}, Sudha Seshadri³², Ramachandran S Vasan^{30

31

33}, Nicholette D Palmer³⁴, Barry I Freedman³⁵, Donald W Bowden³⁴, Lisa R Yanek³⁶, Brian G Kral³⁶, Lewis C Becker³⁶, Patricia A Peyser³⁷, Lawrence F Bielak³⁷, Farah Ammous³⁷, April P Carson³⁸, Michael E Hall³⁸, Laura M Raffield³⁹, Stephen S Rich⁴⁰, Wendy S Post⁴¹, Russel P Tracy⁴², Kent D Taylor⁴³, Xiuqing Guo⁴³, Michael C Mahaney⁴⁴, Joanne E Curran⁴⁴, John Blangero⁴⁴, Shoa L Clarke^{45

46

47}, Jeffrey W Haessler⁴⁸, Yao Hu⁴⁸, Themistocles L Assimes^{45

46

47}, Charles Kooperberg⁴⁸, Jürgen Bernhagen^{4

49

50}, Christopher D Anderson^{10

11

12}, Scott M Damrauer^{8

9

51}, Ramin Zand^{52

53}, Jerome I Rotter⁴³, Paul S de Vries⁵, Martin Dichgans^{54

55

56

57}

Affiliations

¹ Institute for Stroke and Dementia Research (ISD), University Hospital, Ludwig-Maximilians-University (LMU), Feodor-Lynen-Str. 17, 81377, Munich, Germany. marios.georgakis@med.uni-muenchen.de.
² Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, Cambridge, MA, USA. marios.georgakis@med.uni-muenchen.de.
³ Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. marios.georgakis@med.uni-muenchen.de.
⁴ Institute for Stroke and Dementia Research (ISD), University Hospital, Ludwig-Maximilians-University (LMU), Feodor-Lynen-Str. 17, 81377, Munich, Germany.
⁵ Human Genetics Center, Department of Epidemiology, School of Public Health, Human Genetics, and Environmental Sciences, the University of Texas Health Science Center at Houston, Houston, TX, USA.
⁶ Department of Molecular and Functional Genomics, Geisinger Health System, Danville, PA, USA.
⁷ Veterans Affairs Healthcare System, Boston, MA, USA.
⁸ Department of Surgery, Perelman School of Medicineat Theaq , University of Pennsylvania, Philadelphia, PA, USA.
⁹ Corporal Michael Crescenz VA Medical Center, Philadelphia, PA, USA.
¹⁰ Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, Cambridge, MA, USA.
¹¹ Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, USA.
¹² Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA.
¹³ Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.
¹⁴ Geriatrics Research and Education Clinical Center, Baltimore Veterans Administration Medical Center, Baltimore, MD, USA.
¹⁵ The Charles Bronfman Institute for Personalized Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
¹⁶ Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
¹⁷ The Center for Genomic Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
¹⁸ Pamela Sklar Division of Psychiatric Genomics, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
¹⁹ Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
²⁰ Department of Radiology, Vanderbilt University Medical Center, Nashville, TN, USA.
²¹ Department of Medicine, Cardiovascular Health Research Unit, University of Washington, Seattle, WA, USA.
²² Department of Health Systems and Population Health, University of Washington, Seattle, WA, USA.
²³ Department of Epidemiology, University of Washington, Seattle, WA, USA.
²⁴ Department of Neurology, University of Washington, Seattle, WA, USA.
²⁵ Department of Epidemiology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
²⁶ Department of Population Medicine, PRecisiOn Medicine Translational Research (PROMoTeR) Center, Harvard Pilgrim Health Careand, Harvard Medical School , Boston, MA, USA.
²⁷ Department of Biostatistics, T.H. Chan School of Public Health, Harvard University, Boston, MA, USA.
²⁸ Channing Division of Network Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
²⁹ Department of Biostatistics, University of Washington, Seattle, WA, USA.
³⁰ Department of Medicine, Boston University School of Medicine, Boston, MA, USA.
³¹ Boston University and National Heart, Blood Institute'S Framingham Heart Study, Lung, and Framingham, MA, USA.
³² Bigg'S Institute for Alzheimer'S Disease and Neurodegenerative Disorders, University of Texas Health Science Center, San Antonio, TX, USA.
³³ Department of Epidemiology, Boston University School of Public Health, Boston, MA, USA.
³⁴ Department of Biochemistry, Wake Forest School of Medicine, Winston-Salem, NC, USA.
³⁵ Section on Nephrology, Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, NC, USA.
³⁶ Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
³⁷ Department of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, MI, USA.
³⁸ Department of Medicine, University of Mississippi Medical Center, Jackson, MS, USA.
³⁹ Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
⁴⁰ Center for Public Health Genomics, University of Virginia, Charlottesville, VA, USA.
⁴¹ Johns Hopkins Bloomberg School of Public Health, Johns Hopkins School of Medicine, Baltimore, MD, USA.
⁴² Departments of Pathology & Laboratory Medicine, and Biochemistry, Larner College of Medicine, University of Vermont, Burlington, VT, USA.
⁴³ The Institute for Translational Genomics and Population Sciences, Department of Pediatrics, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, CA, USA.
⁴⁴ Department of Human Genetics and South Texas Diabetes and Obesity Institute, University of Texas Rio Grande Valley School of Medicine, Brownsville, TX, USA.
⁴⁵ Department of Medicine (Division of Cardiovascular Medicine), Stanford University School of Medicine, Stanford, CA, USA.
⁴⁶ Stanford Cardiovascular Institute, Stanford, CA, USA.
⁴⁷ VA Palo Alto Health Care System, Palo Alto, CA, USA.
⁴⁸ Division of Public Health Sciences, Fred Hutchinson Cancer Center, Seattle, WA, 98109, USA.
⁴⁹ Munich Cluster for Systems Neurology (SyNergy), Munich, Germany.
⁵⁰ German Centre for Cardiovascular Research (DZHK, Munich), Partner Site Munich Heart Alliance, Munich, Germany.
⁵¹ Department of Genetics, Perelman School of Medicineat the , University of Pennsylvania, Philadelphia, PA, USA.
⁵² Department of Neurology, Pennsylvania State University, Hershey, PA, USA.
⁵³ Department of Neurology, Neuroscience Institute, Geisinger Health System, Danville, PA, USA.
⁵⁴ Institute for Stroke and Dementia Research (ISD), University Hospital, Ludwig-Maximilians-University (LMU), Feodor-Lynen-Str. 17, 81377, Munich, Germany. martin.dichgans@med.uni-muenchen.de.
⁵⁵ Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. martin.dichgans@med.uni-muenchen.de.
⁵⁶ German Centre for Neurodegenerative Diseases (DZNE), Munich, Germany. martin.dichgans@med.uni-muenchen.de.
⁵⁷ German Centre for Cardiovascular Research (DZHK, Munich), Partner Site Munich Heart Alliance, Munich, Germany. martin.dichgans@med.uni-muenchen.de.

^# Contributed equally.

PMID: 40119478
PMCID: PMC11929344
DOI: 10.1186/s13073-025-01456-2

Rare damaging CCR2 variants are associated with lower lifetime cardiovascular risk

Marios K Georgakis et al. Genome Med. 2025.

. 2025 Mar 21;17(1):27.

doi: 10.1186/s13073-025-01456-2.

Authors

Affiliations

¹ Institute for Stroke and Dementia Research (ISD), University Hospital, Ludwig-Maximilians-University (LMU), Feodor-Lynen-Str. 17, 81377, Munich, Germany. marios.georgakis@med.uni-muenchen.de.
² Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, Cambridge, MA, USA. marios.georgakis@med.uni-muenchen.de.
³ Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. marios.georgakis@med.uni-muenchen.de.
⁴ Institute for Stroke and Dementia Research (ISD), University Hospital, Ludwig-Maximilians-University (LMU), Feodor-Lynen-Str. 17, 81377, Munich, Germany.
⁵ Human Genetics Center, Department of Epidemiology, School of Public Health, Human Genetics, and Environmental Sciences, the University of Texas Health Science Center at Houston, Houston, TX, USA.
⁶ Department of Molecular and Functional Genomics, Geisinger Health System, Danville, PA, USA.
⁷ Veterans Affairs Healthcare System, Boston, MA, USA.
⁸ Department of Surgery, Perelman School of Medicineat Theaq , University of Pennsylvania, Philadelphia, PA, USA.
⁹ Corporal Michael Crescenz VA Medical Center, Philadelphia, PA, USA.
¹⁰ Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, Cambridge, MA, USA.
¹¹ Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, USA.
¹² Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA.
¹³ Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.
¹⁴ Geriatrics Research and Education Clinical Center, Baltimore Veterans Administration Medical Center, Baltimore, MD, USA.
¹⁵ The Charles Bronfman Institute for Personalized Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
¹⁶ Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
¹⁷ The Center for Genomic Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
¹⁸ Pamela Sklar Division of Psychiatric Genomics, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
¹⁹ Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
²⁰ Department of Radiology, Vanderbilt University Medical Center, Nashville, TN, USA.
²¹ Department of Medicine, Cardiovascular Health Research Unit, University of Washington, Seattle, WA, USA.
²² Department of Health Systems and Population Health, University of Washington, Seattle, WA, USA.
²³ Department of Epidemiology, University of Washington, Seattle, WA, USA.
²⁴ Department of Neurology, University of Washington, Seattle, WA, USA.
²⁵ Department of Epidemiology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
²⁶ Department of Population Medicine, PRecisiOn Medicine Translational Research (PROMoTeR) Center, Harvard Pilgrim Health Careand, Harvard Medical School , Boston, MA, USA.
²⁷ Department of Biostatistics, T.H. Chan School of Public Health, Harvard University, Boston, MA, USA.
²⁸ Channing Division of Network Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
²⁹ Department of Biostatistics, University of Washington, Seattle, WA, USA.
³⁰ Department of Medicine, Boston University School of Medicine, Boston, MA, USA.
³¹ Boston University and National Heart, Blood Institute'S Framingham Heart Study, Lung, and Framingham, MA, USA.
³² Bigg'S Institute for Alzheimer'S Disease and Neurodegenerative Disorders, University of Texas Health Science Center, San Antonio, TX, USA.
³³ Department of Epidemiology, Boston University School of Public Health, Boston, MA, USA.
³⁴ Department of Biochemistry, Wake Forest School of Medicine, Winston-Salem, NC, USA.
³⁵ Section on Nephrology, Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, NC, USA.
³⁶ Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
³⁷ Department of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, MI, USA.
³⁸ Department of Medicine, University of Mississippi Medical Center, Jackson, MS, USA.
³⁹ Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
⁴⁰ Center for Public Health Genomics, University of Virginia, Charlottesville, VA, USA.
⁴¹ Johns Hopkins Bloomberg School of Public Health, Johns Hopkins School of Medicine, Baltimore, MD, USA.
⁴² Departments of Pathology & Laboratory Medicine, and Biochemistry, Larner College of Medicine, University of Vermont, Burlington, VT, USA.
⁴³ The Institute for Translational Genomics and Population Sciences, Department of Pediatrics, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, CA, USA.
⁴⁴ Department of Human Genetics and South Texas Diabetes and Obesity Institute, University of Texas Rio Grande Valley School of Medicine, Brownsville, TX, USA.
⁴⁵ Department of Medicine (Division of Cardiovascular Medicine), Stanford University School of Medicine, Stanford, CA, USA.
⁴⁶ Stanford Cardiovascular Institute, Stanford, CA, USA.
⁴⁷ VA Palo Alto Health Care System, Palo Alto, CA, USA.
⁴⁸ Division of Public Health Sciences, Fred Hutchinson Cancer Center, Seattle, WA, 98109, USA.
⁴⁹ Munich Cluster for Systems Neurology (SyNergy), Munich, Germany.
⁵⁰ German Centre for Cardiovascular Research (DZHK, Munich), Partner Site Munich Heart Alliance, Munich, Germany.
⁵¹ Department of Genetics, Perelman School of Medicineat the , University of Pennsylvania, Philadelphia, PA, USA.
⁵² Department of Neurology, Pennsylvania State University, Hershey, PA, USA.
⁵³ Department of Neurology, Neuroscience Institute, Geisinger Health System, Danville, PA, USA.
⁵⁴ Institute for Stroke and Dementia Research (ISD), University Hospital, Ludwig-Maximilians-University (LMU), Feodor-Lynen-Str. 17, 81377, Munich, Germany. martin.dichgans@med.uni-muenchen.de.
⁵⁵ Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. martin.dichgans@med.uni-muenchen.de.
⁵⁶ German Centre for Neurodegenerative Diseases (DZNE), Munich, Germany. martin.dichgans@med.uni-muenchen.de.
⁵⁷ German Centre for Cardiovascular Research (DZHK, Munich), Partner Site Munich Heart Alliance, Munich, Germany. martin.dichgans@med.uni-muenchen.de.

^# Contributed equally.

PMID: 40119478
PMCID: PMC11929344
DOI: 10.1186/s13073-025-01456-2

Abstract

Background: Previous work has shown a role of CCL2, a key chemokine governing monocyte trafficking, in atherosclerosis. However, it remains unknown whether targeting CCR2, the cognate receptor of CCL2, provides protection against human atherosclerotic cardiovascular disease.

Methods: Computationally predicted damaging or loss-of-function (REVEL > 0.5) variants within CCR2 were detected in whole-exome-sequencing data from 454,775 UK Biobank participants and tested for association with cardiovascular endpoints in gene-burden tests. Given the key role of CCR2 in monocyte mobilization, variants associated with lower monocyte count were prioritized for experimental validation. The response to CCL2 of human cells transfected with these variants was tested in migration and cAMP assays. Validated damaging variants were tested for association with cardiovascular endpoints, atherosclerosis burden, and vascular risk factors. Significant associations were replicated in six independent datasets (n = 1,062,595).

Results: Carriers of 45 predicted damaging or loss-of-function CCR2 variants (n = 787 individuals) were at lower risk of myocardial infarction and coronary artery disease. One of these variants (M249K, n = 585, 0.15% of European ancestry individuals) was associated with lower monocyte count and with both decreased downstream signaling and chemoattraction in response to CCL2. While M249K showed no association with conventional vascular risk factors, it was consistently associated with a lower risk of myocardial infarction (odds ratio [OR]: 0.66, 95% confidence interval [CI]: 0.54-0.81, p = 6.1 × 10^-5) and coronary artery disease (OR: 0.74, 95%CI: 0.63-0.87, p = 2.9 × 10^-4) in the UK Biobank and in six replication cohorts. In a phenome-wide association study, there was no evidence of a higher risk of infections among M249K carriers.

Conclusions: Carriers of an experimentally confirmed damaging CCR2 variant are at a lower lifetime risk of myocardial infarction and coronary artery disease without carrying a higher risk of infections. Our findings provide genetic support for the translational potential of CCR2-targeting as an atheroprotective approach.

Keywords: Atherosclerosis; CCR2; Cardiovascular disease; Genetics; Inflammation.

PubMed Disclaimer

Conflict of interest statement

Declarations. Ethics approval and consent to participate: All studies have received ethical approvals from the respective ethical authorities and participants in all studies have provided written informed consent. Data from the UKB are available upon submission and approval of a research proposal. The UKB has institutional review board approval from the Northwest Multi‐Center Research Ethics Committee (Manchester, UK). deCODE has been approved by the National Bioethics Committee of Iceland, and the study was conducted in agreement with conditions issued by the Data Protection Authority of Iceland (VSN_14-015). All common research protocols for the TOPMed Program have been approved by the institutional review board at the University of Maryland Baltimore, whereas individual participating studies have obtained ethical approval from their local ethical authorities, as described previously [60]. The Penn Medicine BioBank is approved by the University of Pennsylvania under IRB protocol# 813913, MVP by the Veterans Affairs Central Institutional Review Board, the Geisinger DiscovEHR-MyCode cohort by Geisinger Institutional Review Boards, and MGBB by the Ethics Committee of Mass General Brigham. Consent for publication: Not applicable. Competing interests: MKG has received consulting fees from Tourmaline Bio Inc., and Gerson Lehrman Group Inc. (unrelated to this work) and is a member of the Editorial Board of Neurology. SMD receives research support from RenalytixAI and personal fees from Calico Labs, both outside the current work. MEM receives funding from Regeneron Pharmaceutical Inc. unrelated to this work. RD has received research support from AstraZeneca and Goldfinch Bio, not related to this work. BMP serves on the Steering Committee of the Yale Open Data Access Program funded by Johnson & Johnson. CDA has received sponsored research support from Bayer AG, has consulted for ApoPharma, and is a member of the Editorial Board of Neurology. LMR is a consultant for the TOPMed Administrative Coordinating Center (through WeStat). The remaining authors have no conflicts of interest to disclose.

Figures

**Fig. 1**
Damaging *CCR2* variants. Domain structure of the CCR2 protein and position of the predicted loss-of-function (LoF) or missense damaging (REVEL > 0.5) variants present in > 2 UK Biobank participants in the *CCR2* exonic regions

**Fig. 2**
Associations of rare computationally predicted damaging *CCR2* variants with risk of atherosclerotic cardiovascular disease in the UK Biobank. Associations of 45 predicted loss-of-function (LoF) or damaging (REVEL > 0.5) *CCR2* variants (minimum allele frequency < 0.01) in burden tests with A risk of cardiovascular disease endpoints and B a combined atherosclerosis endpoint as well as severe clinical atherosclerotic disease defined by manifestations in at least 2 vascular beds (coronary arteries, cerebrovascular system, peripheral arteries of extremities, aorta) among UK Biobank participants of European ancestry. C Prevalence of clinically manifest atherosclerosis across 4 vascular beds (coronary arteries, cerebrovascular system, peripheral arteries of extremities, aorta) among carriers and non-carriers of the 45 predicted LoF or damaging CCR2 variants. The odds ratio (OR) is derived from ordinal regression adjusted for age, sex, and the first 5 ancestral principal components

**Fig. 3**
Validation of the damaging effect of M249K (3:46,358,273:T:A) on CCL2-driven monocyte chemotaxis. A Experimental outline of chemotaxis assay. Transfected CCR2 − / − THP-1 cells (marked in green) and non-transfected cells (marked in red) were used in a Transwell chemotaxis assay. The cells that moved to the lower chamber were collected, stained, and quantified using flow cytometry. B Chemotaxis in response to increasing concentrations of CCL2 for human *CCR2*-knockout monocytic THP-1 cells transfected with the mutant M249K vs. wild-type CCR2, as determined in a trans-well migration assay (comparisons derived from two-way ANOVA, ns: p > 0.05, ***p < 0.001, ****p < 0.0001). C Results of cyclic AMP (cAMP) assay. Shown is the cAMP activity in HEK293T cells transfected with either empty vector or wild-type or M249K *CCR2* in response to different concentrations of CCL2. Results are presented as “Ratio 665/620 × 10,000” (ratio of fluorescence at 665 nm and 620 nm × 10,000). D Associations of M249K with counts of different leukocyte populations in the subset of European ancestry participants of the UK Biobank (N = 393,838), as derived from linear regression models adjusted for age, sex, and the first 5 ancestral principal components

**Fig. 4**
Association of the damaging M249K *CCR2* variant with lifetime cardiovascular risk. Associations of the M249K *CCR2* variant with risk of A cardiovascular disease endpoints, B a combined atherosclerosis endpoint and severe clinical atherosclerotic disease defined by manifestations in at least 2 vascular beds (coronary arteries, cerebrovascular system, peripheral arteries of extremities, aorta), and C conventional vascular risk biomarkers in models adjusted for age, sex, and the first five principal components among UK Biobank participants of European ancestry. HbA1c and C-reactive protein levels are log-transformed for normalization. Fixed-effects and random-effects meta-analysis of the effects of M249K on risk of D myocardial infarction and E coronary artery disease across 7 population- and hospital-based biobanks. The effects correspond to odds ratios (OR) derived from logistic regression models adjusted for age, sex, and the first 5 ancestral principal components in each biobank

**Fig. 5**
Phenome-wide association study of the damaging M249K *CCR2* variant and associations with overall survival. A Results from a phenome-wide association study in UK Biobank and the Geisinger DiscovEHR-MyCode cohort for the M249K *CCR2* variant among participants of European ancestry. Only phecodes with ≥ 10 cases in UK Biobank were analyzed. We present the names of phenotypes associated with rare CCR2 variants at p < 0.05. Only myocardial infarction reached an FDR-corrected p value of < 0.05. The results are presented as log-odds ratios (log-OR). B Kaplan–Meier curves for overall survival across 15 years of follow-up among carriers and non-carriers of the M249K *CCR2* variant in the European subset of UK Biobank participants

See this image and copyright information in PMC

Update of

Rare damaging CCR2 variants are associated with lower lifetime cardiovascular risk.
Georgakis MK, Malik R, El Bounkari O, Hasbani NR, Li J, Huffman JE, Shakt G, Tack RWP, Kimball TN, Asare Y, Morrison AC, Tsao NL, Judy R, Mitchell BD, Xu H, Montasser ME, Do R, Kenny EE, Loos RJF, Terry JG, Carr JJ, Bis JC, Psaty BM, Longstreth WT, Young KA, Lutz SM, Cho MH, Broome J, Khan AT, Wang FF, Heard-Costa N, Seshadri S, Vasan RS, Palmer ND, Freedman BI, Bowden DW, Yanek LR, Kral BG, Becker LC, Peyser PA, Bielak LF, Ammous F, Carson AP, Hall ME, Raffield LM, Rich SS, Post WS, Tracy RP, Taylor KD, Guo X, Mahaney MC, Curran JE, Blangero J, Clarke SL, Haessler JW, Hu Y, Assimes TL, Kooperberg C, Bernhagen J, Anderson CD, Damrauer SM, Zand R, Rotter JI, de Vries PS, Dichgans M. Georgakis MK, et al. medRxiv [Preprint]. 2024 Jun 26:2023.08.14.23294063. doi: 10.1101/2023.08.14.23294063. medRxiv. 2024. Update in: Genome Med. 2025 Mar 21;17(1):27. doi: 10.1186/s13073-025-01456-2. PMID: 37645892 Free PMC article. Updated. Preprint.

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Rare damaging CCR2 variants are associated with lower lifetime cardiovascular risk

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Rare damaging CCR2 variants are associated with lower lifetime cardiovascular risk

Authors

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Abstract

Conflict of interest statement

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