ArticleNephrology (Carlton, Vic.)2025
Revisiting Glomerulopathy in Clusterin Knockout Mice: A Mouse Model of Human Immunotactoid Glomerulopathy.
Article in Nephrology (Carlton, Vic.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Revisiting Glomerulopathy in Clusterin Knockout Mice: A Mouse Model of Human Immunotactoid Glomerulopathy.Nephrology (Carlton, Vic.) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
aimClusterin (CLU) is a chaperone-like glycoprotein, and CLU knockout (KO) mice spontaneously develop age-dependent glomerulopathy with microtubule formation. However, its clinical relevance has not been confirmed yet. Immunotactoid glomerulopathy (ITG) is a clinicopathologic entity of glomerulonephritis characterised by glomerular deposits of electron dense microtubules. This study was to re-examine the glomerulopathy in CLU KO mice as compared with the pathological features of human ITG.
methodsKidney specimens from both wild type C57BL/6 (B6) and CLU-KO B6 mice were analyzed with haematoxylin and eosin, Masson-Trichrome, and Congo-red staining. IgG and DNAJB9 were detected by immunohistochemical staining, and the electron-dense mesangial deposits by transmission electron microscopy. Proteins were identified by liquid chromatography-mass spectrometry.
resultsThere were approximately 75% of glomeruli affected by moderate to severe mesangial lesions in 24-month-old male CLU-KO mice or 85% in 18-month-old female KO mice as compared with little or no glomerular pathology in WT mice at a similar age. The mesangial lesions were stained strongly positive with Masson-Trichrome-stained fibrosis, immunocomplex and anti-IgG, weakly positive with Congo-red, and negative with anti-DNAJB9 antibodies. The electron-dense material in the mesangium was structured with hollow microtubules with an average diameter of 50 nm. Functional enrichments with the STRING database revealed that secreted CLU-bound proteins mainly mediated complement activation and were associated with glomerulonephritis development.
conclusionOur data confirm that the glomerulopathy in CLU-KO B6 mice was similar to the pathological features of ITG and may therefore be considered as an experimental model of ITG. Further, CLU may negatively regulate the fibrillogenesis of ITG.
Indexed as
Identifiers
What Socratic 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 Socratic graph.