Evidence map›Paper›PMID 10194473›Full record

ArticleThe Journal of clinical investigation1999

Aldose reductase functions as a detoxification system for lipid peroxidation products in vasculitis.

H L Rittner, V Hafner, P A Klimiuk, L I Szweda, J J Goronzy, C M Weyand

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
10.5field-weighted citation impact, top 1% 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

59 citing papers in PubMed, 206 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Immunology of Giant Cell Arteritis.Circulation research · 2023
    Review
  6. International journal of biological sciences · 2023
    Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Glucose Metabolism in Cardiac Hypertrophy and Heart Failure.Journal of the American Heart Association · 2019
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 3 institutions in 1 country.

H L RittnerDepartment of Medicine, Division of Rheumatology, Mayo Clinic, Rochester, Minnesota 55905, USA.
V Hafner
P A Klimiuk
L I Szweda
J J Goronzy
C M Weyand
Mayo Clinic in Arizona · USMayo Clinic · USCase Western Reserve University · US

Funding

OCULAR DISEASE IN GIANT CELL ARTERITISR01EY011916 · NEI · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 1997 to 2011
$2.9M
METHOTREXATE EFFECTS IN RHEUMATOID ARTHRITISF05TW005204 · FIC · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI KLIMIUK, PIOTR A · 1995 to 1996
–
FIC NIH HHS F05 TW005204FIC NIH HHS F05 TWO5204NEI NIH HHS R01 EY011916NEI NIH HHS R01 EY 11916
6 · The paper itself

Abstract

Giant cell arteritis (GCA) is a systemic vasculitis preferentially affecting large and medium-sized arteries. Inflammatory infiltrates in the arterial wall induce luminal occlusion with subsequent ischemia and degradation of the elastic membranes, allowing aneurysm formation. To identify pathways relevant to the disease process, differential display-PCR was used. The enzyme aldose reductase (AR), which is implicated in the regulation of tissue osmolarity, was found to be upregulated in the arteritic lesions. Upregulated AR expression was limited to areas of tissue destruction in inflamed arteries, where it was detected in T cells, macrophages, and smooth muscle cells. The production of AR was highly correlated with the presence of 4-hydroxynonenal (HNE), a toxic aldehyde and downstream product of lipid peroxidation. In vitro exposure of mononuclear cells to HNE was sufficient to induce AR production. The in vivo relationship of AR and HNE was explored by treating human GCA temporal artery-severe combined immunodeficiency (SCID) mouse chimeras with the AR inhibitors Sorbinil and Zopolrestat. Inhibition of AR increased HNE adducts twofold and the number of apoptotic cells in the arterial wall threefold. These data demonstrate that AR has a tissue-protective function by preventing damage from lipid peroxidation. We propose that AR is an oxidative defense mechanism able to neutralize the toxic effects of lipid peroxidation and has a role in limiting the arterial wall injury mediated by reactive oxygen species.

Indexed as

ImidazolidinesLipid PeroxidationAldehyde ReductaseAldehydesAnimalsApoptosisBenzothiazolesChimeraEnzyme InhibitorsFree Radical ScavengersGiant Cell ArteritisHumansImidazolesMiceMice, SCIDPhthalazines4-hydroxy-2-nonenalAldehyde ReductaseAldehydesBenzothiazolesEnzyme InhibitorsFree Radical ScavengersImidazolesImidazolidinesPhthalazinesRNA, MessengersorbinilThiazoleszopolrestat

Identifiers

PMID10194473
PMCPMC408253
OpenAlexW1996182204

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.