Evidence map›Paper›PMID 11173607›Full record

ArticlePathology oncology research : POR1996

Aggrecan: A Target Molecule of Autoimmune Reactions.

Edit I Buzás, Katalin Mikecz, Tibor T Glant

Abstract read
PubMed Publisher
In one paragraph

Article in Pathology oncology research : POR, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact, top 86% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Proteasome Inhibitors: Potential in Rheumatoid Arthritis Therapy?International journal of molecular sciences · 2025
    Review
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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

3 authors at 2 institutions in 2 countries.

Edit I BuzásUniversity of Medicine, The Institute of Anatomy, Histology and Embryology, Debrecen, Hungary.
Katalin Mikecz
Tibor T Glant
Rush University Medical Center · USUniversity of Debrecen · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aggrecan in cartilage forms aggregates with hyaluronan and link protein, embedded in a collagen network. It accounts for the compressive stiffness and resilience of the hyaline cartilage. Many forms of inflammatory arthritis were shown to be accompanied with aggrecan degradation and loss from the cartilage. The loss of this major component of cartilage renders the tissue more vulnerable when exposed to abrasive forces. Therefore, aggrecan degradation may significantly contribute to cartilage destruction in arthritis. Furthermore, fragments of degraded aggrecan are released during joint inflammation. Thus, molecules of an avascular, immune-privileged tissue (hyaline cartilage) may become accessible to the cells of the immune system. Similarly, there is a "leakage" of aggrecan fragments from cartilage during aging and after joint injury, which may also lead to autosensibilisation. Autoimmune reactivity to aggrecan can be detected in human joint diseases, as well as in animal models of arthritis. The epitopes involved in these processes are currently being identified. Recent data from work with mice suggest a strong immune response focused to the N-terminal G1 domain of aggrecan that leads to arthritis and spondylitis.

Identifiers

PMID11173607
OpenAlexW2059477442

What OpenQuestion holds

Textmetadata
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.