ReviewJournal of clinical medicine2022
New Insights into the Pathogenesis of Giant Cell Arteritis: Mechanisms Involved in Maintaining Vascular Inflammation.
Review in Journal of clinical medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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
26 citing papers in PubMed, 52 citations in OpenAlex.
- Large vessel vasculitis reframed: integrating conceptual shifts and evidence into practice for Takayasu arteritis and giant cell arteritis.Journal of rheumatic diseases · 2026Review
- Article
- Immunosenescence in Older Patients with Psoriasis: Mechanistic Insights and Opportunities for Biologic Therapy.Psoriasis (Auckland, N.Z.) · 2026Review
- Musculoskeletal ultrasound findings in GCA with PMR and isolated PMR.Rheumatology advances in practice · 2026Article
- Frequency, diagnosis, and pharmacological treatment of giant cell arteritis in Germany: database analysis of medical insurance data.Therapeutic advances in musculoskeletal disease · 2026Article
- Microvascular Health as a Key Determinant of Organismal Aging.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Article
- Association between antibiotic use and the onset of giant cell arteritis and polymyalgia rheumatica: A nested case-control study from E3N-European Prospective Investigation into Cancer and Nutrition.Journal of internal medicine · 2025Article
- Mature CD209Scientific reports · 2025Article
- Uncovering the New Biology of Giant Cell Arteritis to Guide Therapeutic Strategies.Journal of clinical medicine · 2025Review
- Distinct landscapes of fibroblast subtypes in arteries of patients with giant cell arteritis.Rheumatology (Oxford, England) · 2025Article
- Efficacy and Safety of Biological Agents in Giant Cell Arteritis: An Updated Meta-Analysis.Avicenna journal of medicine · 2025Review
- CD6 in Human Disease.Cells · 2025Review
- 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
- Rituximab for antibody-negative combined central and peripheral demyelination presenting with acute respiratory failure: a case report and literature review.Frontiers in immunology · 2025Review
- The Set up and the Triggers: An Update on the Risk Factors for Giant Cell Arteritis.Current neurology and neuroscience reports · 2024Review
- mTOR signalling controls the formation of smooth muscle cell-derived luminal myofibroblasts during vasculitis.EMBO reports · 2024Article
- Management of Coronary Artery Diseases in Systemic Vasculitides: Complications and Strategies.Medicina (Kaunas, Lithuania) · 2024Review
- Diagnostic accuracy of serum biomarkers to identify giant cell arteritis in patients with polymyalgia rheumatica.RMD open · 2024Article
- Ultrasound Examination of Common Carotid Adventitial Thickness Can Differentiate Takayasu Arteritis and Large Vessel Giant Cell Arteritis.Journal of personalized medicine · 2024Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The giant cell arteritis (GCA) pathophysiology is complex and multifactorial, involving a predisposing genetic background, the role of immune aging and the activation of vascular dendritic cells by an unknown trigger. Once activated, dendritic cells recruit CD4 T cells and induce their activation, proliferation and polarization into Th1 and Th17, which produce interferon-gamma (IFN-γ) and interleukin-17 (IL-17), respectively. IFN-γ triggers the production of chemokines by vascular smooth muscle cells, which leads to the recruitment of additional CD4 and CD8 T cells and also monocytes that differentiate into macrophages. Recent data have shown that IL-17, IFN-γ and GM-CSF induce the differentiation of macrophage subpopulations, which play a role in the destruction of the arterial wall, in neoangiogenesis or intimal hyperplasia. Under the influence of different mediators, mainly endothelin-1 and PDGF, vascular smooth muscle cells migrate to the intima, proliferate and change their phenotype to become myofibroblasts that further proliferate and produce extracellular matrix proteins, increasing the vascular stenosis. In addition, several defects in the immune regulatory mechanisms probably contribute to chronic vascular inflammation in GCA: a defect in the PD-1/PD-L1 pathway, a quantitative and qualitative Treg deficiency, the implication of resident cells, the role of GM-CSF and IL-6, the implication of the NOTCH pathway and the role of mucosal-associated invariant T cells and tissue-resident memory T cells.
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.