Evidence mapPaperPMID 11865066Full record

ArticleMolecular and cellular biology2002

Apolipoprotein J/clusterin prevents a progressive glomerulopathy of aging.

Mark E Rosenberg, Richard Girton, David Finkel, David Chmielewski, Arthur Barrie, David P Witte, Guang Zhu, John J Bissler, Judith A K Harmony, Bruce J Aronow

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01524705 (FLAT-SUGAR), which is not on this map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
1.9field-weighted citation impact, top 14% 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.

NCT01524705 phase4completedstarted 2012, after this paper: background citation

FLAT-SUGAR: FLuctuATion Reduction With inSULin and Glp-1 Added togetheR

Ran2012Enrolled102Registered outcomes4Posted comparisons3ConditionsType 2 DiabetesArmsexenatide, Insulin glargine, Metformin, Prandial insulin
Open the trial in the graph
3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 112 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Clusterin, other extracellular chaperones, and eye disease.Progress in retinal and eye research · 2022
    Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  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

10 authors at 1 institution in 1 country.

Mark E RosenbergDivision of Renal Diseases and Hypertension, Department of Medicine, University of Minnesota, UMHC 736, 516 Delaware Street SE, Minneapolis, MN 55455, USA. rosen001@umn.edu
Richard Girton
David Finkel
David Chmielewski
Arthur Barrie
David P Witte
Guang Zhu
John J Bissler
Judith A K Harmony
Bruce J Aronow
University of Minnesota · US

Funding

CLUSTERIN AND RENAL INJURYR01DK048452 · UNIVERSITY OF MINNESOTA TWIN CITIES · 1996 to 2004
$1.3M
REGULATION OF AN EXTRACELLULAR XENOBIOTIC RESPONSE GENER01ES008822 · CHILDREN'S HOSPITAL MED CTR (CINCINNATI) · 1997 to 1999
NIDDK NIH HHS R01 DK048452NIDDK NIH HHS R01 DK 48452NIEHS NIH HHS R01 ES 08822
6 · The paper itself

Abstract

Apoliprotein J (apoJ)/clusterin has attracted considerable interest based on its inducibility in multiple injury processes and accumulation at sites of remodeling, regression, and degeneration. We therefore sought to investigate apoJ/clusterin's role in kidney aging, as this may reveal the accumulated effects of diminished protection. Aging mice deficient in apoJ/clusterin developed a progressive glomerulopathy characterized by the deposition of immune complexes in the mesangium. Up to 75% of glomeruli in apoJ/clusterin-deficient mice exhibited moderate to severe mesangial lesions by 21 months of age. Wild-type and hemizygous mice exhibited little or no glomerular pathology. In the apoJ/clusterin-deficient mice, immune complexes of immunoglobulin G (IgG), IgM, IgA, and in some cases C1q, C3, and C9 were detectable as early as 4 weeks of age. Electron microscopy revealed the accumulation of electron-dense material in the mesangial matrix and age-dependent formation of intramesangial tubulo-fibrillary structures. Even the most extensively damaged glomeruli showed no evidence of inflammation or necrosis. In young apoJ/clusterin-deficient animals, the development of immune complex lesions was accelerated by unilateral nephrectomy-induced hyperfiltration. Injected immune complexes localized to the mesangium of apoJ/clusterin-deficient but not wild-type mice. These results establish a protective role of apoJ/clusterin against chronic glomerular kidney disease and support the hypothesis that apoJ/clusterin modifies immune complex metabolism and disposal.

Indexed as

AgingAnimalsAntigen-Antibody ComplexClusterinComplement System ProteinsDisease ProgressionGlomerular MesangiumGlomerulonephritis, MembranoproliferativeGlycoproteinsHeterozygoteHomozygoteImmunoglobulinsKidney GlomerulusMiceMice, KnockoutMolecular ChaperonesAntigen-Antibody ComplexClu protein, mouseClusterinComplement System ProteinsGlycoproteinsImmunoglobulinsMolecular Chaperones

Identifiers

PMID11865066
PMCPMC135592
OpenAlexW2113743289

What Socratic holds

Textmetadata
Read underepoch 390

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 Socratic graph.