Evidence map›Paper›PMID 26977416›Full record

ArticleJournal of diabetes research2016

Increased Autoreactivity of the Complement-Activating Molecule Mannan-Binding Lectin in a Type 1 Diabetes Model.

Jakob Appel Østergaard, Marieta Milkova Ruseva, Talat Habib Malik, Ingeborg Torp Hoffmann-Petersen, Matthew Caleb Pickering, Steffen Thiel, Troels Krarup Hansen

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of diabetes research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Observational
  9. Article
  10. Review
  11. Review
  12. Article
  13. Endothelial heparan sulfate deficiency reduces inflammation and fibrosis in murine diabetic nephropathy.Laboratory investigation; a journal of technical methods and pathology · 2018
    Article
  14. Review
  15. Article
  16. 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

7 authors at 5 institutions in 2 countries.

Jakob Appel ØstergaardDepartment of Endocrinology and Internal Medicine, Aarhus University Hospital and Department of Clinical Medicine, Faculty of Health, Aarhus University, 8000 Aarhus, Denmark; The Danish Diabetes Academy, 5000 Odense, Denmark.
Marieta Milkova RusevaCentre for Complement and Inflammation Research, Imperial College London, London W12 0NN, UK.
Talat Habib MalikCentre for Complement and Inflammation Research, Imperial College London, London W12 0NN, UK.
Ingeborg Torp Hoffmann-PetersenDepartment of Endocrinology and Internal Medicine, Aarhus University Hospital and Department of Clinical Medicine, Faculty of Health, Aarhus University, 8000 Aarhus, Denmark.
Matthew Caleb PickeringCentre for Complement and Inflammation Research, Imperial College London, London W12 0NN, UK.
Steffen ThielDepartment of Biomedicine, Faculty of Health, Aarhus University, 8000 Aarhus, Denmark.
Troels Krarup HansenDepartment of Endocrinology and Internal Medicine, Aarhus University Hospital and Department of Clinical Medicine, Faculty of Health, Aarhus University, 8000 Aarhus, Denmark.
Aarhus University Hospital · DKImperial College London · GBAarhus University · DKCentre for Inflammation Research · GBDanish Diabetes Academy · DK

Funding

Wellcome TrustWellcome Trust WT082291MA
6 · The paper itself

Abstract

backgroundDiabetic kidney disease is the leading cause of end-stage renal failure despite intensive treatment of modifiable risk factors. Identification of new drug targets is therefore of paramount importance. The complement system is emerging as a potential new target. The lectin pathway of the complement system, initiated by the carbohydrate-recognition molecule mannan-binding lectin (MBL), is linked to poor kidney prognosis in diabetes. We hypothesized that MBL activates complement upon binding within the diabetic glomerulus.

methodsWe investigated this by comparing complement deposition and activation in kidneys from streptozotocin-induced diabetic mice and healthy control mice.

resultsAfter 20 weeks of diabetes, glomerular deposition of MBL was significantly increased. Diabetic animals had 2.0-fold higher (95% CI 1.6-2.5) immunofluorescence intensity from anti-MBL antibodies compared with controls (P < 0.001). Diabetes and control groups did not differ in glomerular immunofluorescence intensity obtained by antibodies against complement factors C4, C3, and C9. However, the circulating complement activation product C3a was increased in diabetes as compared to control mice (P = 0.04).

conclusion20 weeks of diabetes increased MBL autoreactivity in the kidney and circulating C3a concentration. Together with previous findings, these results indicate direct effects of MBL within the kidney in diabetes.

Indexed as

Complement ActivationComplement Pathway, Mannose-Binding LectinAnimalsBlood GlucoseComplement C3aDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Diabetic NephropathiesKidney GlomerulusMaleMannose-Binding LectinMice, Inbred C57BLBlood GlucoseComplement C3aMannose-Binding Lectin

Identifiers

PMID26977416
PMCPMC4764751
OpenAlexW2269693048

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.