Evidence map›Paper›PMID 25722732›Full record

ArticleDrug discovery today. Disease models2014

Lupus Nephritis: Animal Modeling of a Complex Disease Syndrome Pathology.

Tracy L McGaha, Michael P Madaio

Abstract read
In one paragraph

Article in Drug discovery today. Disease models, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-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.

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

14 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  6. Article
  7. Review
  8. Mesenchymal stem cells: A new therapeutic tool for chronic kidney disease.Frontiers in cell and developmental biology · 2022
    Review
  9. Review
  10. A systems approach to renal inflammation in SLE.Clinical immunology (Orlando, Fla.) · 2017
    Review
  11. Article
  12. Review
  13. Review
  14. 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

2 authors at 2 institutions in 1 country.

Tracy L McGahaCancer Immunology, Inflammation, and Tolerance Program. GRU Cancer Center. Georgia Regents University ; Department of Medicine, Division of Nephrology, Medical College of Georgia. Georgia Regents University.
Michael P MadaioDepartment of Medicine, Division of Nephrology, Medical College of Georgia. Georgia Regents University.
Augusta University · USGeorgia Regents Medical Center · US

Funding

Modified Human Anti-a(3) IV Antibodies for Drug Delivery in NephritisR21DK081140 · NIDDK · AUGUSTA UNIVERSITY · PI MADAIO, MICHAEL P · 2009 to 2010
$404k
The role of GCN2-kinase in antigen presenting cell function and tolerance to selfR21AI105500 · NIAID · AUGUSTA UNIVERSITY · PI MCGAHA, TRACY L · 2013 to 2014
$399k
Mechanisms of marginal zone macrophage mediated tolerance towards apoptotic cellR56AI099043 · NIAID · AUGUSTA UNIVERSITY · PI MCGAHA, TRACY L · 2013 to 2013
$353k
The role of indoleamine 2-3 dioxygenase in marginal zone-mediated toleranceR56AI092213 · NIAID · AUGUSTA UNIVERSITY · PI MCGAHA, TRACY L · 2011 to 2011
$335k
NIAID NIH HHS R21 AI105500NIAID NIH HHS R56 AI092213NIAID NIH HHS R56 AI099043NIDDK NIH HHS R21 DK081140
6 · The paper itself

Abstract

Nephritis as a result of autoimmunity is a common morbidity associated with Systemic Lupus Erythematosus (SLE). There is substantial clinical and industry interest in medicinal intervention in the SLE nephritic process; however, clinical trials to specifically treat lupus nephritis have not resulted in complete and sustained remission in all patients. Multiple mouse models have been used to investigate the pathologic interactions between autoimmune reactivity and SLE pathology. While several models bear a remarkable similarity to SLE-driven nephritis, there are limitations for each that can make the task of choosing the appropriate model for a particular aspect of SLE pathology challenging. This is not surprising given the variable and diverse nature of human disease. In many respects, features among murine strains mimic some (but never all) of the autoimmune and pathologic features of lupus patients. Although the diversity often limits universal conclusions relevant to pathogenesis, they provide insights into the complex process that result in phenotypic manifestations of nephritis. Thus nephritis represents a microcosm of systemic disease, with variable lesions and clinical features. In this review, we discuss some of the most commonly used models of lupus nephritis (LN) and immune-mediated glomerular damage examining their relative strengths and weaknesses, which may provide insight in the human condition.

Identifiers

PMID25722732
PMCPMC4337231
OpenAlexW2066519552

What OpenQuestion holds

Textmetadata
LicenceTDM
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.