ArticleJournal of hypertension2009
Cross-sectional relations of multiple biomarkers representing distinct biological pathways to plasma markers of collagen metabolism in the community.
Article in Journal of hypertension, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Preprocedural Biomarkers of Inflammation and Fibrosis and Echocardiographic Markers of Myocardial Remodeling in New-Onset Conduction Disorders After Transcatheter Aortic Valve Implantation.Medicina (Kaunas, Lithuania) · 2026Observational
- Homocysteine promotes cardiac fibrosis by regulating the Akt/FoxO3 pathway.Annals of translational medicine · 2021Article
- Association Between Inflammatory Markers and Myocardial Fibrosis.Hypertension (Dallas, Tex. : 1979) · 2018Article
- Methoxistasis: integrating the roles of homocysteine and folic acid in cardiovascular pathobiology.Nutrients · 2013Review
- Effects of direct Renin inhibition on myocardial fibrosis and cardiac fibroblast function.PloS one · 2013Article
- Soluble guanylate cyclase stimulation prevents fibrotic tissue remodeling and improves survival in salt-sensitive Dahl rats.PloS one · 2011Article
- Relations of biomarkers of extracellular matrix remodeling to incident cardiovascular events and mortality.Arteriosclerosis, thrombosis, and vascular biology · 2010Article
- Quo vadis: whither homocysteine research?Cardiovascular toxicology · 2009Review
Corrections and comments
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Authors and funding
11 authors at 7 institutions in 1 country.
Funding
Abstract
objectiveHyperhomocysteinemia, neurohormonal activation, inflammation and altered fibrinolysis have been linked to atherothrombosis as well as to myocardial fibrosis and heart failure. Hence, we related a panel of biomarkers representing these pathways to plasma markers of collagen metabolism in a large community-based sample.
methodsWe related nine biomarkers representing select biologic pathways (independent variables: C-reactive protein, B-type natriuretic peptide, N-terminal proatrial natriuretic peptide, aldosterone, renin, fibrinogen, D-dimer, plasminogen activator inhibitor-1 and homocysteine) to three plasma markers of collagen turnover [dependent variables, separate models for each: aminoterminal propeptide of type III collagen, tissue inhibitor of metalloproteinases-1 and matrix metalloproteinase-9 (present versus absent)] in 921 Framingham Heart study participants (mean age 57 years; 58% women). Participants were separated a priori into those with left ventricular end-diastolic dimensions and wall thickness below sex-specific median values (referent group) and either measure at least 90th sex-specific percentile ('remodeled' group). We used stepwise multivariable regression analysis adjusting for cardiovascular risk factors to relate the panel of systemic biomarkers to the three biomarkers of collagen metabolism.
resultsPlasma homocysteine was positively related to all three markers of collagen metabolism in the remodeled group and to aminoterminal propeptide of type III collagen and tissue inhibitor of metalloproteinases-1 in the referent group. Plasminogen activator inhibitor-1 was positively related to aminoterminal propeptide of type III collagen and tissue inhibitor of metalloproteinases-1 in both groups, whereas the natriuretic peptides were associated positively with these collagen markers in the referent group.
conclusionIn our large community-based sample, plasma homocysteine and plasminogen activator inhibitor-1 were positively related to circulating collagen biomarkers, consistent with experimental studies implicating these pathways in cardiovascular collagen turnover.
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