ReviewAutoimmunity2009
Vascular damage in giant cell arteritis.
Review in Autoimmunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- A meta-analysis of the epidemiology of giant cell arteritis across time and space.Arthritis research & therapy · 2021Pooled it
- Automated detection of giant cell arteritis from temporal artery biopsy specimens using deep learning approaches.Scientific reports · 2026Article
- Increased expression of Toll-like receptors and associated alarmins in temporal arteries of patients with giant cell arteritis.Molecular medicine (Cambridge, Mass.) · 2025Article
- Causal genes identification of giant cell arteritis in CD4+ Memory t cells: an integration of multi-omics and expression quantitative trait locus analysis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Pathogenesis of Pulmonary Manifestations in ANCA-Associated Vasculitis and Goodpasture Syndrome.International journal of molecular sciences · 2024Review
- Review
- Current Perspectives in Giant Cell Arteritis: Can We Better Connect Pathogenesis and Treatment?Medicina (Kaunas, Lithuania) · 2024Review
- Review
- Deficiency of the CD155-CD96 immune checkpoint controls IL-9 production in giant cell arteritis.Cell reports. Medicine · 2023Article
- New Insights into the Pathogenesis of Giant Cell Arteritis: Mechanisms Involved in Maintaining Vascular Inflammation.Journal of clinical medicine · 2022Review
- The innate face of Giant Cell Arteritis: Insight into cellular and molecular innate immunity pathways to unravel new possible biomarkers of disease.Frontiers in molecular medicine · 2022Review
- Stroke secondary to giant-cell arteritis: A literature review.Experimental and therapeutic medicine · 2021Article
- Dysregulated Expression of Arterial MicroRNAs and Their Target Gene Networks in Temporal Arteries of Treatment-Naïve Patients with Giant Cell Arteritis.International journal of molecular sciences · 2021Article
- NOTCH-induced rerouting of endosomal trafficking disables regulatory T cells in vasculitis.The Journal of clinical investigation · 2021Article
- CD28 Signaling Controls Metabolic Fitness of Pathogenic T Cells in Medium and Large Vessel Vasculitis.Journal of the American College of Cardiology · 2019Article
- Bioinformatics identification of potential candidate blood indicators for doxorubicin-induced heart failure.Experimental and therapeutic medicine · 2018Article
- Recent Advances in Giant Cell Arteritis.Current rheumatology reports · 2018Review
- The microvascular niche instructs T cells in large vessel vasculitis via the VEGF-Jagged1-Notch pathway.Science translational medicine · 2017Article
- Hydroxysafflor yellow A inhibits lipopolysaccharide-induced proliferation and migration of vascular smooth muscle cells via Toll-like receptor-4 pathway.International journal of clinical and experimental medicine · 2015Article
- Vascular involvement in cardiac giant cell myocarditis: a new pathophysiological aspect.Clinical research in cardiology : official journal of the German Cardiac Society · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Immune-mediated damage to medium-sized arteries results in wall remodeling with intimal hyperplasia, luminal stenosis and tissue ischemia. In the case of the aorta, vasculitis may result in dissection, aneurysm or rupture. The response-to-injury program of the blood vessel is a concerted action between the immune system and wall-resident cells, involving the release of growth and angiogenic factors from macrophages and giant cells and the migration and hyperproliferation of vascular smooth muscle cells. Innate immune cells, specifically, dendritic cells (DC) positioned in the vessel wall, have been implicated in the earliest steps of vasculitis. Pathogen-derived molecular patterns are capable of activating vascular DC and initiating adaptive immune responses. The pattern of the emerging vessel wall inflammation is ultimately determined by the initial insult. Ligands to toll-like receptor (TLR) 4, such as lipopolysaccharides, facilitate the recruitment of CD4 T cells that invade deep into the wall and distribute in a panarteritic pattern. Conversely, ligands for TLR5 condition vascular DC to support perivasculitic infiltrates. In essence, both innate and adaptive immune reactions collaborate to render the arterial wall susceptible to inflammatory damage. Unique features of the tissue microenvironment, including specialized DC, shape the course of the inflammatory response. Differences in vascular damage pattern encountered in different patients may relate to distinct instigators of vasculitis.
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.