ArticleThe American journal of pathology2006
Identification of differential protein expression associated with development of unstable human carotid plaques.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- BRCA2 variants and cardiovascular disease in a multi-ethnic study.BMC medical genetics · 2012Pooled it
- Searching for Atherosclerosis Biomarkers by Proteomics: A Focus on Lesion Pathogenesis and Vulnerability.International journal of molecular sciences · 2023Review
- Macrophage Phenotyping in Atherosclerosis by Proteomics.International journal of molecular sciences · 2023Review
- The Role of Tumor Necrosis Factor Associated Factors (TRAFs) in Vascular Inflammation and Atherosclerosis.Frontiers in cardiovascular medicine · 2022Review
- Advances in Cardiovascular Biomarker Discovery.Biomedicines · 2020Review
- Article
- Targeting Opposing Immunological Roles of the Junctional Adhesion Molecule-A in Autoimmunity and Cancer.Frontiers in immunology · 2020Review
- JNK and NF-κB signaling pathways are involved in cytokine changes in patients with congenital heart disease prior to and after transcatheter closure.Experimental and therapeutic medicine · 2018Article
- Anti-JNK2 peptide-siRNA nanostructures improve plaque endothelium and reduce thrombotic risk in atherosclerotic mice.International journal of nanomedicine · 2018Article
- Article
- Secreted proteins from carotid endarterectomy: an untargeted approach to disclose molecular clues of plaque progression.Journal of translational medicine · 2013Article
- Atherosclerosis, platelets and thrombosis in acute ischaemic heart disease.European heart journal. Acute cardiovascular care · 2012Article
- Gene expression differences between stroke-associated and asymptomatic carotid plaques.Journal of molecular medicine (Berlin, Germany) · 2011Article
- Transcription and translation of human F11R gene are required for an initial step of atherogenesis induced by inflammatory cytokines.Journal of translational medicine · 2011Article
- GPCR kinase 2 interacting protein 1 (GIT1) regulates osteoclast function and bone mass.Journal of cellular physiology · 2010Article
- C-reactive protein exerts angiogenic effects on vascular endothelial cells and modulates associated signalling pathways and gene expression.BMC cell biology · 2008Article
- Proteomic Biomarkers of Atherosclerosis.Biomarker insights · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rupture-prone unstable arterial plaques develop concomitantly with the appearance of intraplaque hemorrhage and tissue ulceration, in association with deregulation of smooth muscle cell mitogenesis and leakage of newly formed blood vessels. Using microarray technology, we have identified novel protein deregulation associated with unstable carotid plaque regions. Overexpression of proapoptotic proteins caspase-9 and TRAF4 was seen in endothelial cells and smooth muscle cells from unstable hemorrhagic and ulcerated plaque regions. Topoisomerase-II-alpha (TOPO-II-alpha), which is associated with DNA repair mechanisms, was also overexpressed by these cells. Cell signaling molecules c-src, G-protein-coupled receptor kinase-interacting protein (GIT1), and c-jun N-terminal kinase (JNK) were up-regulated in endothelial cells from the same areas, whereas an increase in expression of junctional adhesion molecule-1 (JAM-1) in blood vessels and infiltrating macrophages from inflammatory regions might form part of a leukocyte rolling response, increasing the plaque volume. Grb2-like adaptor protein (Gads), responsible for differentiation of monocytes into macrophages, was expressed by macrophages from unstable plaques, suggesting a potential mechanism through which increased scavenging could occur in rupture-prone areas. We conclude that modulation of novel cell signaling intermediates, such as those described here, could be useful in the therapy of angiogenesis and apoptosis, designed to reduce unstable plaque formation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.