Evidence map›Paper›PMID 38474394›Full record

ReviewCells2024

Current Insights into Tissue Injury of Giant Cell Arteritis: From Acute Inflammatory Responses towards Inappropriate Tissue Remodeling.

Dimitris Anastasios Palamidas, Loukas Chatzis, Maria Papadaki, Ilias Gissis, Konstantinos Kambas, Evangelos Andreakos, Andreas V Goules, Athanasios G Tzioufas

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
3.4field-weighted citation impact, top 8% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 8 citations in OpenAlex.

  1. Suspected ophthalmic artery fat embolus following bilateral elbow liposuction.American journal of ophthalmology case reports · 2026
    Article
  2. Proceedings of the 2Mediterranean journal of rheumatology · 2026
    Article
  3. Contribution ofCurrent issues in molecular biology · 2025
    Review
  4. Observational
  5. Review
  6. Article
  7. Article
  8. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Dimitris Anastasios PalamidasDepartment of Pathophysiology, School of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece.
Loukas ChatzisDepartment of Pathophysiology, School of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece.ORCID 0000-0002-2832-0116
Maria PapadakiLaboratory of Immunobiology, Center for Clinical, Experimental Surgery and Translational Research, Biomedical Research Foundation of the Academy of Athens, 11527 Athens, Greece.
Ilias GissisDepartment of Thoracic and Cardiovascular Surgery, Evangelismos General Hospital, 11473 Athens, Greece.
Konstantinos KambasLaboratory of Molecular Genetics, Department of Immunology, Hellenic Pasteur Institute, 11521 Athens, Greece.
Evangelos AndreakosLaboratory of Immunobiology, Center for Clinical, Experimental Surgery and Translational Research, Biomedical Research Foundation of the Academy of Athens, 11527 Athens, Greece.
Andreas V GoulesDepartment of Pathophysiology, School of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece.ORCID 0000-0003-4343-0396
Athanasios G TzioufasDepartment of Pathophysiology, School of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece.ORCID 0000-0001-6666-8642
National and Kapodistrian University of Athens · GRAcademy of Athens · GREvangelismos Hospital · GRPasteur Hellenic Institute · GR

Funding

European Union 779295George and Victoria Karelias Foundation donation
6 · The paper itself

Abstract

Giant cell arteritis (GCA) is an autoimmune disease affecting large vessels in patients over 50 years old. It is an exemplary model of a classic inflammatory disorder with IL-6 playing the leading role. The main comorbidities that may appear acutely or chronically are vascular occlusion leading to blindness and thoracic aorta aneurysm formation, respectively. The tissue inflammatory bulk is expressed as acute or chronic delayed-type hypersensitivity reactions, the latter being apparent by giant cell formation. The activated monocytes/macrophages are associated with pronounced Th1 and Th17 responses. B-cells and neutrophils also participate in the inflammatory lesion. However, the exact order of appearance and mechanistic interactions between cells are hindered by the lack of cellular and molecular information from early disease stages and accurate experimental models. Recently, senescent cells and neutrophil extracellular traps have been described in tissue lesions. These structures can remain in tissues for a prolonged period, potentially favoring inflammatory responses and tissue remodeling. In this review, current advances in GCA pathogenesis are discussed in different inflammatory phases. Through the description of these-often overlapping-phases, cells, molecules, and small lipid mediators with pathogenetic potential are described.

Indexed as

Giant Cell ArteritisB-LymphocytesHumansInflammationMacrophagesMiddle AgedNeutrophilsgiant cell arteritismonocytespathogenetic mechanismsenescencetissue injurytissue remodeling

Identifiers

PMID38474394
PMCPMC10930978
OpenAlexW4392286502

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.