Evidence map›Paper›PMID 31608060›Full record

ArticleFrontiers in immunology2019

Absence of the Lectin Activation Pathway of Complement Ameliorates Proteinuria-Induced Renal Injury.

Samy Alghadban, Hany I Kenawy, Thomas Dudler, Wilhelm J Schwaeble, Nigel J Brunskill

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Prevalence and Therapies of Antibiotic-Resistance inFrontiers in cellular and infection microbiology · 2020
    Review
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

5 authors at 3 institutions in 3 countries.

Samy AlghadbanDepartment of Infection, Immunity and Inflammation, College of Life Sciences, University of Leicester, Leicester, United Kingdom.
Hany I KenawyDepartment of Infection, Immunity and Inflammation, College of Life Sciences, University of Leicester, Leicester, United Kingdom.
Thomas DudlerOmeros Corporation, Seattle, WA, United States.
Wilhelm J SchwaebleDepartment of Infection, Immunity and Inflammation, College of Life Sciences, University of Leicester, Leicester, United Kingdom.
Nigel J BrunskillDepartment of Infection, Immunity and Inflammation, College of Life Sciences, University of Leicester, Leicester, United Kingdom.
University of Leicester · GBMansoura University · EGOmeros Corporation (United States) · US

Funding

Medical Research Council G0700859Medical Research Council G0801952Medical Research Council G1000191
6 · The paper itself

Abstract

Proteinuria is an adverse prognostic feature in renal diseases. In proteinuric nephropathies, filtered proteins exert an injurious effect on the renal tubulointerstitium, resulting in inflammation and fibrosis. In the present study, we assessed to what extent complement activation via the lectin pathway may contribute to renal injury in response to proteinuria-related stress in proximal tubular cells. We used the well-established mouse model of protein overload proteinuria (POP) to assess the effect of lectin pathway inhibition on renal injury and fibrotic changes characteristic of proteinuric nephropathy. To this end, we compared experimental outcomes in wild type mice with MASP-2-deficient mice or wild type mice treated with MASP-2 inhibitor to block lectin pathway functional activity. Multiple markers of renal injury were assessed including renal function, proteinuria, macrophage infiltration, and cytokine release profiles. Both MASP-2-deficient and MASP-2 inhibitor-treated wild type mice exhibited renoprotection from proteinuria with significantly less tubulointerstitial injury when compared to isotype control antibody treated mice. This indicates that therapeutic targeting of MASP-2 in proteinuric nephropathies may offer a useful strategy in the clinical management of proteinuria associated pathologies in a variety of different underlying renal diseases.

Indexed as

AnimalsComplement ActivationComplement System ProteinsCytokinesFibrosisKidneyKidney DiseasesLectinsMacrophagesMaleMannose-Binding Protein-Associated Serine ProteasesMiceMice, Inbred BALB CProteinuriaSignal TransductionComplement System ProteinsCytokinesLectinsMannose-Binding Protein-Associated Serine Proteaseskidneylectin pathwayMASPMBL-associated serine proteasesnephropathyproteinuria

Identifiers

PMID31608060
PMCPMC6768126
OpenAlexW2972127807

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.