Cited by 18Aortic aneurysm repair treatmentsConnective tissue disorders researchGenetic Associations and Epidemiology

Proteomics Analysis of Genetic Liability of Abdominal Aortic Aneurysm Identifies Plasma Neogenin and Kit Ligand: The ARIC Study

Open access
Steffen, Brian T., Pankow, James S., Norby, Faye L., Lutsey, Pamela L., Demmer, Ryan T., Guan, Weihua, Pankratz, Nathan, Li, Aixin +4 more·2023·Arteriosclerosis, Thrombosis, and Vascular Biology

Abstract

Background: Genome-wide association studies have reported 23 gene loci related to abdominal aortic aneurysm (AAA)—a potentially lethal condition characterized by a weakened dilated vessel wall. This study aimed to identify proteomic signatures and pathways related to these risk loci to better characterize AAA genetic susceptibility. Methods: Plasma concentrations of 4870 proteins were determined using a DNA aptamer-based array. Linear regression analysis estimated the associations between the 23 risk alleles and plasma protein levels with adjustments for potential confounders in a race-stratified analysis of 1671 Black and 7241 White participants. Significant proteins were then evaluated for their prediction of clinical AAA (454 AAA events in 11 064 individuals), and those significantly associated with AAA were further interrogated using Mendelian randomization analysis. Results: Risk variants proximal to PSRC1-CELSR2-SORT1 , PCIF1-ZNF335-MMP9, RP11-136O12.2/TRIB1 , ZNF259/APOA5, IL6R , PCSK9 , LPA , and APOE were associated with 118 plasma proteins in Whites and 59 were replicated in Black participants. Novel associations with clinical AAA incidence were observed for kit ligand (HR, 0.59 [95% CI, 0.42–0.82] for top versus first quintiles) and neogenin (HR, 0.64 [95% CI, 0.46–0.88]) over a median 21.2-year follow-up; neogenin was also associated with ultrasound-detected asymptomatic AAA (N=4295; 57 asymptomatic AAA cases). Mendelian randomization inverse variance weighted estimates suggested that AAA risk is promoted by lower levels of kit ligand (OR per SD=0.67; P =1.4×10 −5 ) and neogenin (OR per SD=0.50; P =0.03). Conclusions: Low levels of neogenin and kit ligand may be novel risk factors for AAA development in potentially causal pathways. These findings provide insights and potential targets to reduce AAA susceptibility.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1161/atvbaha.122.317984

Cites

2 of 2 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • ZPR1/rs964184 has been implicated in the LXR/RXR activation pathway that affected the expression and plasma level of ApoE, along with ApoA1, ApoA5, and ApoC3.

    “Since the submission of our manuscript, ZPR1/rs964184 has been implicated in the LXR/RXR activation pathway that affected the expression and plasma level of ApoE, along with ApoA1, ApoA5 and ApoC3 [41].”

    From Genome-wide analysis identifies novel loci influencing plasma apolipoprotein E concentration and Alzheimer’s disease risk (2023) · cites this paper as [41]

    The Results (Pathway analysis; page unavailable) link rs964184, labeled ZNF259/APOA5, to LXR/RXR activation. The Results (Associations of proteins and AAA-related SNPs; page unavailable) also report an association with plasma apolipoprotein A-V. Our copy does not establish effects on gene expression or specifically link rs964184 to plasma ApoE, ApoA1, or ApoC3. (LLM, conf=0.87)

    Experimental — accuracy not yet measured
  • rs964184 has been associated with triglycerides, type 2 diabetes, and abdominal aortic aneurysm.

    “has been associated with triglycerides [39, 40], type 2 diabetes [39] and abdominal aortic aneurysm (AAA) [41].”
  • The cited finding provides confirmation to our independent observation and affirms the association of ZPR1/rs964184 with ApoE level being genuine.

    “This provides confirmation to our independent observation and affirms the association of ZPR1/rs964184 with ApoE level being genuine.”

    From Genome-wide analysis identifies novel loci influencing plasma apolipoprotein E concentration and Alzheimer’s disease risk (2023) · cites this paper as [41]

    The Results section, “Associations of proteins and AAA-related SNPs” (page unavailable), reports that rs964184 was associated with 33 plasma proteins, highlighting apolipoprotein A-V and protein phosphatase inhibitor 2. Neither that passage nor the additional passages searched for rs964184 and apolipoprotein E establish an association with ApoE levels; the paper discusses an APOE-linked variant, rs429358, separately. (LLM, conf=0.70)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 50

  1. [1]Takayama T, Yamanouchi D. Aneurysmal disease: the abdominal aorta. Surg Clin North Am. 2013; 93: 877– 891, viii. doi: 10.1016/j.suc.2013.05.005 23885935 · DOI
  2. [2]Tang W, Yao L, Roetker NS, Alonso A, Lutsey PL, Steenson CC, Lederle FA, Hunter DW, Bengtson LG, Guan W, Lifetime Risk and Risk Factors for Abdominal Aortic Aneurysm in a 24-Year Prospective Study: The ARIC Study (Atherosclerosis Risk in Communities). Arterioscler Thromb Vasc Biol. 2016; 36: 2468– 2477. doi: 10.1161/atvbaha.116.308147 27834688 PMC5397388 · DOI
  3. [3]Folsom AR, Yao L, Alonso A, Lutsey PL, Missov E, Lederle FA, Ballantyne CM, Tang W. Circulating Biomarkers and Abdominal Aortic Aneurysm Incidence: The Atherosclerosis Risk in Communities (ARIC) Study. Circulation. 2015; 132: 578– 585. doi: 10.1161/circulationaha.115.016537 26085454 PMC4543558 · DOI
  4. [4]Bruijn LE, van Stroe Gómez CG, Curci JA, Golledge J, Hamming JF, Jones GT, Lee R, Matic L, van Rhijn C, Vriens PW, A histopathological classification scheme for abdominal aortic aneurysm disease. JVS Vasc Sci. 2021; 2: 260– 273. doi: 10.1016/j.jvssci.2021.09.001 34825232 PMC8605212 · DOI
  5. [5]Tang W, Yao L, Hoogeveen RC, Alonso A, Couper DJ, Lutsey PL, Steenson CC, Guan W, Hunter DW, Lederle FA, The Association of Biomarkers of Inflammation and Extracellular Matrix Degradation With the Risk of Abdominal Aortic Aneurysm: The ARIC Study. Angiology. 2019; 70: 130– 140. doi: 10.1177/0003319718785278 29945457 PMC6810681 · DOI
  6. [6]Dale MA, Ruhlman MK, Baxter BT. Inflammatory cell phenotypes in AAAs: their role and potential as targets for therapy. Arterioscler Thromb Vasc Biol. 2015; 35: 1746– 1755. doi: 10.1161/atvbaha.115.305269 26044582 PMC4514552 · DOI
  7. [7]Sénémaud J, Caligiuri G, Etienne H, Delbosc S, Michel JB, Coscas R. Translational Relevance and Recent Advances of Animal Models of Abdominal Aortic Aneurysm. Arterioscler Thromb Vasc Biol. 2017; 37: 401– 410. doi: 10.1161/atvbaha.116.308534 28062500 · DOI
  8. [8]Larsson E, Granath F, Swedenborg J, Hultgren R. A population-based case-control study of the familial risk of abdominal aortic aneurysm. J Vasc Surg. 2009; 49: 47– 50; discussion 51. doi: 10.1016/j.jvs.2008.08.012 19028058 · DOI
  9. [9]Ogata T, MacKean GL, Cole CW, Arthur C, Andreou P, Tromp G, Kuivaniemi H. The lifetime prevalence of abdominal aortic aneurysms among siblings of aneurysm patients is eightfold higher than among siblings of spouses: an analysis of 187 aneurysm families in Nova Scotia, Canada. J Vasc Surg. 2005; 42: 891– 897. doi: 10.1016/j.jvs.2005.08.002 16275443 PMC1373672 · DOI
  10. [10]Joergensen TM, Christensen K, Lindholt JS, Larsen LA, Green A, Houlind K. Editor ’s Choice - High Heritability of Liability to Abdominal Aortic Aneurysms: A Population Based Twin Study. Eur J Vasc Endovasc Surg. 2016; 52: 41– 46. doi: 10.1016/j.ejvs.2016.03.012 27107486 · DOI
  11. [11]Wahlgren CM, Larsson E, Magnusson PK, Hultgren R, Swedenborg J. Genetic and environmental contributions to abdominal aortic aneurysm development in a twin population. J Vasc Surg. 2010; 51: 3– 7; discussion 7. doi: 10.1016/j.jvs.2009.08.036 19939604 · DOI
  12. [12]Shibamura H, Olson JM, van Vlijmen-Van Keulen C, Buxbaum SG, Dudek DM, Tromp G, Ogata T, Skunca M, Sakalihasan N, Pals G, Genome scan for familial abdominal aortic aneurysm using sex and family history as covariates suggests genetic heterogeneity and identifies linkage to chromosome 19q13. Circulation. 2004; 109: 2103– 2108. doi: 10.1161/01.Cir.0000127857.77161.A1 15096456 · DOI
  13. [13]Gretarsdottir S, Baas AF, Thorleifsson G, Holm H, den Heijer M, de Vries JP, Kranendonk SE, Zeebregts CJ, van Sterkenburg SM, Geelkerken RH, Genome-wide association study identifies a sequence variant within the DAB2IP gene conferring susceptibility to abdominal aortic aneurysm. Nat Genet. 2010; 42: 692– 697. doi: 10.1038/ng.622 20622881 PMC4157066 · DOI
  14. [14]Klarin D, Verma SS, Judy R, Dikilitas O, Wolford BN, Paranjpe I, Levin MG, Pan C, Tcheandjieu C, Spin JM, Genetic Architecture of Abdominal Aortic Aneurysm in the Million Veteran Program. Circulation. 2020; 142: 1633– 1646. doi: 10.1161/circulationaha.120.047544 32981348 PMC7580856 · DOI
  15. [15]Jones GT, Tromp G, Kuivaniemi H, Gretarsdottir S, Baas AF, Giusti B, Strauss E, Van’t Hof FN, Webb TR, Erdman R, Meta-Analysis of Genome-Wide Association Studies for Abdominal Aortic Aneurysm Identifies Four New Disease-Specific Risk Loci. Circ Res. 2017; 120: 341– 353. doi: 10.1161/circresaha.116.308765 27899403 PMC5253231 · DOI
  16. [16]Wright JD, Folsom AR, Coresh J, Sharrett AR, Couper D, Wagenknecht LE, Mosley TH Jr., Ballantyne CM, Boerwinkle EA, Rosamond WD, The ARIC (Atherosclerosis Risk In Communities) Study: JACC Focus Seminar 3/8. J Am Coll Cardiol. 2021; 77: 2939– 2959. doi: 10.1016/j.jacc.2021.04.035 34112321 PMC8667593 · DOI
  17. [17]Pankow JS, Tang W, Pankratz N, Guan W, Weng LC, Cushman M, Boerwinkle E, Folsom AR. Identification of Genetic Variants Linking Protein C and Lipoprotein Metabolism: The ARIC Study (Atherosclerosis Risk in Communities). Arterioscler Thromb Vasc Biol. 2017; 37: 589– 597. doi: 10.1161/atvbaha.116.308109 28082259 PMC5376064 · DOI
  18. [18]Taliun D, Harris DN, Kessler MD, Carlson J, Szpiech ZA, Torres R, Taliun SAG, Corvelo A, Gogarten SM, Kang HM, Sequencing of 53,831 diverse genomes from the NHLBI TOPMed Program. Nature. 2021; 590: 290– 299. doi: 10.1038/s41586-021-03205-y 33568819 PMC7875770 · DOI · Paper page
  19. [19]Byun J, Han Y, Gorlov IP, Busam JA, Seldin MF, Amos CI. Ancestry inference using principal component analysis and spatial analysis: a distance-based analysis to account for population substructure. BMC Genomics. 2017; 18: 789. doi: 10.1186/s12864-017-4166-8 29037167 PMC5644186 · DOI
  20. [20]Inker LA, Schmid CH, Tighiouart H, Eckfeldt JH, Feldman HI, Greene T, Kusek JW, Manzi J, Van Lente F, Zhang YL, Estimating glomerular filtration rate from serum creatinine and cystatin C. N Engl J Med. 2012; 367: 20– 29. doi: 10.1056/NEJMoa1114248 22762315 PMC4398023 · DOI · Paper page
  21. [21]Ballew SH, Chen Y, Daya NR, Godino JG, Windham BG, McAdams-DeMarco M, Coresh J, Selvin E, Grams ME. Frailty, Kidney Function, and Polypharmacy: The Atherosclerosis Risk in Communities (ARIC) Study. Am J Kidney Dis. 2017; 69: 228– 236. doi: 10.1053/j.ajkd.2016.08.034 27884475 PMC5263025 · DOI
  22. [22]Grubb A, Blirup-Jensen S, Lindström V, Schmidt C, Althaus H, Zegers I. First certified reference material for cystatin C in human serum ERM-DA471/IFCC. Clin Chem Lab Med. 2010; 48: 1619– 1621. doi: 10.1515/cclm.2010.318 21034257 · DOI
  23. [23]Gold L, Walker JJ, Wilcox SK, Williams S. Advances in human proteomics at high scale with the SOMAscan proteomics platform. N Biotechnol. 2012; 29: 543– 549. doi: 10.1016/j.nbt.2011.11.016 22155539 · DOI
  24. [24]Kim CH, Tworoger SS, Stampfer MJ, Dillon ST, Gu X, Sawyer SJ, Chan AT, Libermann TA, Eliassen AH. Stability and reproducibility of proteomic profiles measured with an aptamer-based platform. Sci Rep. 2018; 8: 8382. doi: 10.1038/s41598-018-26640-w 29849057 PMC5976624 · DOI · Paper page
  25. [25]Han Z, Xiao Z, Kalantar-Zadeh K, Moradi H, Shafi T, Waikar SS, Quarles LD, Yu Z, Tin A, Coresh J, Validation of a Novel Modified Aptamer-Based Array Proteomic Platform in Patients with End-Stage Renal Disease. Diagnostics (Basel). 2018; 8. doi: 10.3390/diagnostics8040071 PMC6316431 30297602 · DOI
  26. [26]Williams SA, Kivimaki M, Langenberg C, Hingorani AD, Casas JP, Bouchard C, Jonasson C, Sarzynski MA, Shipley MJ, Alexander L, Plasma protein patterns as comprehensive indicators of health. Nat Med. 2019; 25: 1851– 1857. doi: 10.1038/s41591-019-0665-2 31792462 PMC6922049 · DOI · Paper page
  27. [27]Tin A, Yu B, Ma J, Masushita K, Daya N, Hoogeveen RC, Ballantyne CM, Couper D, Rebholz CM, Grams ME, Reproducibility and Variability of Protein Analytes Measured Using a Multiplexed Modified Aptamer Assay. J Appl Lab Med. 2019; 4: 30– 39. doi: 10.1373/jalm.2018.027086 31639705 PMC6814271 · DOI · Paper page
  28. [28]Gottesman RF, Rawlings AM, Sharrett AR, Albert M, Alonso A, Bandeen-Roche K, Coker LH, Coresh J, Couper DJ, Griswold ME, Impact of differential attrition on the association of education with cognitive change over 20 years of follow-up: the ARIC neurocognitive study. Am J Epidemiol. 2014; 179: 956– 966. doi: 10.1093/aje/kwu020 24627572 PMC3966720 · DOI
  29. [30]Roychowdhury T KD, Levin MG, Spin JM, Rhee YH, Deng A Multi-ancestry GWAS deciphers genetic architecture of abdominal aortic aneurysm and highlights PCSK9 as a therapeutic target. medRxiv. 2022;2022.05.27.22275607. doi: 10.1101/2022.05.27.22275607 · DOI
  30. [31]Choi Y, Lee SJ, Spiller W, Jung KJ, Lee JY, Kimm H, Back JH, Lee S, Jee SH. Causal Associations Between Serum Bilirubin Levels and Decreased Stroke Risk: A Two-Sample Mendelian Randomization Study. Arterioscler Thromb Vasc Biol. 2020; 40: 437– 445. doi: 10.1161/atvbaha.119.313055 31801373 PMC6975519 · DOI
  31. [32]Krämer A, Green J, Pollard J, Jr., Tugendreich S. Causal analysis approaches in Ingenuity Pathway Analysis. Bioinformatics. 2014; 30: 523– 530. doi: 10.1093/bioinformatics/btt703 24336805 PMC3928520 · DOI · Paper page
  32. [33]van der Harst P, Verweij N. Identification of 64 Novel Genetic Loci Provides an Expanded View on the Genetic Architecture of Coronary Artery Disease. Circ Res. 2018; 122: 433– 443. doi: 10.1161/circresaha.117.312086 29212778 PMC5805277 · DOI · Paper page
  33. [34]Ryer EJ, Garvin RP, Schworer CM, Bernard-Eckroth KR, Tromp G, Franklin DP, Elmore JR, Kuivaniemi H. Proinflammatory role of stem cells in abdominal aortic aneurysms. J Vasc Surg. 2015; 62: 1303– 1311.e1304. doi: 10.1016/j.jvs.2014.04.067 24997808 · DOI
  34. [35]Kim JY, Choi JS, Song SH, Im JE, Kim JM, Kim K, Kwon S, Shin HK, Joo CK, Lee BH, Stem cell factor is a potent endothelial permeability factor. Arterioscler Thromb Vasc Biol. 2014; 34: 1459– 1467. doi: 10.1161/atvbaha.114.303575 24790137 · DOI
  35. [36]Song L, Martinez L, Zigmond ZM, Hernandez DR, Lassance-Soares RM, Selman G, Vazquez-Padron RI. c-Kit modifies the inflammatory status of smooth muscle cells. PeerJ. 2017; 5: e3418. doi: 10.7717/peerj.3418 28626608 PMC5472039 · DOI
  36. [37]Song L, Zigmond ZM, Martinez L, Lassance-Soares RM, Macias AE, Velazquez OC, Liu ZJ, Salama A, Webster KA, Vazquez-Padron RI. c-Kit suppresses atherosclerosis in hyperlipidemic mice. Am J Physiol Heart Circ Physiol. 2019; 317: H867– h876. doi: 10.1152/ajpheart.00062.2019 31441677 PMC6843012 · DOI
  37. [38]Sakaue S, Kanai M, Tanigawa Y, Karjalainen J, Kurki M, Koshiba S, Narita A, Konuma T, Yamamoto K, Akiyama M, A cross-population atlas of genetic associations for 220 human phenotypes. Nat Genet. 2021; 53: 1415– 1424. doi: 10.1038/s41588-021-00931-x 34594039 PMC12208603 · DOI
  38. [39]Hadi T, Boytard L, Silvestro M, Alebrahim D, Jacob S, Feinstein J, Barone K, Spiro W, Hutchison S, Simon R, Macrophage-derived netrin-1 promotes abdominal aortic aneurysm formation by activating MMP3 in vascular smooth muscle cells. Nat Commun. 2018; 9: 5022. doi: 10.1038/s41467-018-07495-1 30479344 PMC6258757 · DOI
  39. [40]Shen L, Wang S, Ling Y, Liang W. Association of C1q/TNF-related protein-1 (CTRP1) serum levels with coronary artery disease. J Int Med Res. 2019; 47: 2571– 2579. doi: 10.1177/0300060519847372 31081425 PMC6567692 · DOI
  40. [41]Lu L, Zhang RY, Wang XQ, Liu ZH, Shen Y, Ding FH, Meng H, Wang LJ, Yan XX, Yang K, C1q/TNF-related protein-1: an adipokine marking and promoting atherosclerosis. Eur Heart J. 2016; 37: 1762– 1771. doi: 10.1093/eurheartj/ehv649 26705391 · DOI
  41. [43]Harrison SC, Smith AJ, Jones GT, Swerdlow DI, Rampuri R, Bown MJ, Folkersen L, Baas AF, de Borst GJ, Blankensteijn JD, Interleukin-6 receptor pathways in abdominal aortic aneurysm. Eur Heart J. 2013; 34: 3707– 3716. doi: 10.1093/eurheartj/ehs354 23111417 PMC3869968 · DOI
  42. [44]Rosa M, Chignon A, Li Z, Boulanger MC, Arsenault BJ, Bossé Y, Thériault S, Mathieu P. A Mendelian randomization study of IL6 signaling in cardiovascular diseases, immune-related disorders and longevity. NPJ Genom Med. 2019; 4: 23. doi: 10.1038/s41525-019-0097-4 31552141 PMC6754413 · DOI
  43. [45]Yan D, Ma H, Shi W, Luo P, Liu T, Guo J, Zhai M, Tao J, Huo S, Li C, Bazedoxifene Attenuates Abdominal Aortic Aneurysm Formation via Downregulation of Interleukin-6/Glycoprotein 130/Signal Transducer and Activator of Transcription 3 Signaling Pathway in Apolipoprotein E-Knockout Mice. Front Pharmacol. 2020; 11: 392. doi: 10.3389/fphar.2020.00392 32362823 PMC7180191 · DOI
  44. [46]Hou T, Tieu BC, Ray S, Recinos Iii A, Cui R, Tilton RG, Brasier AR. Roles of IL-6-gp130 Signaling in Vascular Inflammation. Curr Cardiol Rev. 2008; 4: 179– 192. doi: 10.2174/157340308785160570 19936194 PMC2780819 · DOI
  45. [47]Sulkava M, Raitoharju E, Mennander A, Levula M, Seppälä I, Lyytikäinen LP, Järvinen O, Illig T, Klopp N, Mononen N, Differentially expressed genes and canonical pathways in the ascending thoracic aortic aneurysm - The Tampere Vascular Study. Sci Rep. 2017; 7: 12127. doi: 10.1038/s41598-017-12421-4 28935963 PMC5608723 · DOI
  46. [48]Maegdefessel L, Azuma J, Toh R, Merk DR, Deng A, Chin JT, Raaz U, Schoelmerich AM, Raiesdana A, Leeper NJ, Inhibition of microRNA-29b reduces murine abdominal aortic aneurysm development. J Clin Invest. 2012; 122: 497– 506. doi: 10.1172/jci61598 22269326 PMC3266800 · DOI
  47. [49]Bhattacharjee S, Jun B, Belayev L, Heap J, Kautzmann MA, Obenaus A, Menghani H, Marcell SJ, Khoutorova L, Yang R, Elovanoids are a novel class of homeostatic lipid mediators that protect neural cell integrity upon injury. Sci Adv. 2017; 3:e1700735. doi: 10.1126/sciadv.1700735 PMC5617374 28959727 · DOI · Paper page
  48. [50]Pham TL, He J, Kakazu AH, Calandria J, Do KV, Nshimiyimana R, Petasis NA, Bazan HEP, Bazan NG. Elovanoid-N32 or RvD6-isomer decrease ACE2 and binding of S protein RBD after injury or INFγ in the eye. Res Sq. 2020. doi: 10.21203/rs.3.rs-55764/v1 · DOI
  49. [51]Calandria JM, Bhattacharjee S, Maness NJ, Kautzmann MI, Asatryan A, Gordon WC, Do KV, Jun B, Mukherjee PK, Petasis NA, Elovanoids downregulate SARS-CoV-2 cell-entry, canonical mediators and enhance protective signaling in human alveolar cells. Sci Rep. 2021; 11: 12324. doi: 10.1038/s41598-021-91794-z 34112906 PMC8192580 · DOI
  50. [52]Pierce BL, Burgess S. Efficient design for Mendelian randomization studies: subsample and 2-sample instrumental variable estimators. Am J Epidemiol. 2013; 178: 1177– 1184. doi: 10.1093/aje/kwt084 23863760 PMC3783091 · DOI · Paper page

Cited by

Sorted by citations

Authors
Steffen, B. T., Pankow, J. S., Norby, F. L., Lutsey, P. L., Demmer, R. T., Guan, W., Pankratz, N., Li, A., Liu, G., Matsushita, K., Tin, A., & Tang, W.
Affiliations
  • University of Minnesota (US)
  • Cedars-Sinai Medical Center (US)
  • The University of Texas Health Science Center at Houston (US)
  • Johns Hopkins University (US)
  • University of Mississippi Medical Center (US)
Venue
Arteriosclerosis, Thrombosis, and Vascular Biology
Published
2023-02
Volume
43
Issue
2
Pages
367-378
ISSN
  • 1079-5642 (ISSN-L)
  • 1524-4636
OpenAlex
W4313279978
Cited by
18
References
2
Citations by year
2026: 9 · 2025: 3 · 2024: 4 · 2023: 2
FWCI
1.45
Type
journal article
Language
en
Open access
Locations
  • Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Heart, Lung, and Blood Institute (HHSN268201700004I, R01HL103695, R01HL155209, HHSN268201700001I, HHSN268201700003I, R01HL087641, R01HL059367, R01HL134320, HHSN268201700001C, HHSN268201700002I, HHSN268201700003C, HHSN268201700002C, HHSN268201700004C, K24HL159246, K01HL164764, T32HL007779, R01HL086694)
  • National Human Genome Research Institute (U01HG004402)
  • National Center for Research Resources (UL1RR025005)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Aortic aneurysm repair treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Connective tissue disorders research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
Keywords
abdominal aortic aneurysm, genetic susceptibility, plasma proteomics, neogenin, stem cell factor, genetic susceptibility loci, asymptomatic aneurysm, Mendelian randomization, aneurysm risk factors
MeSH terms
Proprotein Convertase 9, Humans, Membrane Proteins, Nuclear Proteins, Risk Factors, Transcription Factors, Protein Serine-Threonine Kinases, Aortic Aneurysm, Abdominal, Stem Cell Factor, Proteomics, Intracellular Signaling Peptides and Proteins, Adaptor Proteins, Signal Transducing, Genome-Wide Association Study

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review