ArticleScientific reports2017
Pentraxin 3, ficolin-2 and lectin pathway associated serine protease MASP-3 as early predictors of myocardial infarction - the HUNT2 study.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- A Systematic Review and Meta-Analysis of Advanced Biomarkers for Predicting Incident Cardiovascular Disease among Asymptomatic Middle-Aged Adults.International journal of molecular sciences · 2022Pooled it
- Extracellular vesicle proteomics uncovers energy metabolism, complement system, and endoplasmic reticulum stress response dysregulation postexercise in males with myalgic encephalomyelitis/chronic fatigue syndrome.Clinical and translational medicine · 2025Article
- Differential gene expression patterns in ST-elevation Myocardial Infarction and Non-ST-elevation Myocardial Infarction.Scientific reports · 2024Article
- The Lectin Pathway of the Complement System-Activation, Regulation, Disease Connections and Interplay with Other (Proteolytic) Systems.International journal of molecular sciences · 2024Review
- The complement system in lipid-mediated pathologies.Frontiers in immunology · 2024Review
- Ficolin-2 amplifies inflammation in macrophage-smooth muscle cell cross-talk and increases monocyte transmigration by mechanisms involving IL-1β and IL-6.Scientific reports · 2023Article
- Status of mannose-binding lectin (MBL) and complement system in COVID-19 patients and therapeutic applications of antiviral plant MBLs.Molecular and cellular biochemistry · 2021Review
- The pattern-recognition molecule H-ficolin in relation to diabetic kidney disease, mortality, and cardiovascular events in type 1 diabetes.Scientific reports · 2021Observational
- Local complement activation is associated with primary graft dysfunction after lung transplantation.JCI insight · 2020Article
- Potential impacts of high-sensitivity creatine kinase-MB on long-term clinical outcomes in patients with stable coronary heart disease.Scientific reports · 2020Article
- Pentraxin 3 in Cardiovascular Disease.Frontiers in immunology · 2019Review
- The prognostic significance of heart-type fatty acid binding protein in patients with stable coronary heart disease.Scientific reports · 2018Article
- Post-myocardial infarction treatment with resiniferatoxin modulates the expression of important genes involved in inflammation, plaque stability and angiogenesis.Discoveries (Craiova, Romania)Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The lectin complement pathway is suggested to play a role in atherogenesis. Pentraxin-3 (PTX3), ficolin-1, ficolin-2, ficolin-3, MBL/ficolin/collectin-associated serine protease-3 (MASP-3) and MBL/ficolin/collectin-associated protein-1 (MAP-1) are molecules related to activation of the lectin complement pathway. We hypothesized that serum levels of these molecules may be associated with the incidence of myocardial infarction (MI). In a Norwegian population-based cohort (HUNT2) where young to middle-aged relatively healthy Caucasians were followed up for a first-time MI from 1995-1997 through 2008, the 370 youngest MI patients were matched by age (range 29-62 years) and gender to 370 controls. After adjustments for traditional risk factors, the two highest tertiles of PTX3 and the highest tertiles of ficolin-2 and MASP-3 were associated with MI, with odds ratios (95% confidence interval) of 1.65 (1.10-2.47) and 2.79 (1.83-4.24) for PTX3, 1.55 (1.04-2.30) for ficolin-2, and 0.63 (0.043-0.94) for MASP-3. Ficolin-1, ficolin-3 and MAP-1 were not associated with MI. In a multimarker analysis of all associated biomarkers, only PTX3 and MASP-3 remained significant. PTX-3 and MASP-3 enhanced prediction of MI compared to the traditional Framingham risk score alone (AUC increased from 0.64 to 0.68, p = 0.006). These results support the role of complement-dependent inflammation in the pathophysiology of cardiovascular disease.
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