Evidence map›Paper›PMID 24498203›Full record

ArticlePloS one2014

Effects of melanocortin 1 receptor agonists in experimental nephropathies.

Annika Lindskog Jonsson, Anna Granqvist, Johannes Elvin, Martin E Johansson, Börje Haraldsson, Jenny Nyström

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. 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
1.8field-weighted citation impact, top 17% 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, 25 citations in OpenAlex.

  1. The Synthetic Melanocortin Agonist NDP-MSH Ameliorates THSD7A-Associated Membranous Nephropathy in an Active Immunization Mouse Model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Melanocortins: A new paradigm in immunotherapy for membranous nephropathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
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  14. The podocyte as a direct target for treatment of glomerular disease?American journal of physiology. Renal physiology · 2016
    Review
  15. Article
  16. Adrenocorticotropic hormone analog use for podocytopathies.International medical case reports journal · 2016
    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

6 authors at 2 institutions in 1 country.

Annika Lindskog JonssonDepartment of Molecular and Clinical Medicine - Nephrology, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Anna GranqvistDepartment of Molecular and Clinical Medicine - Nephrology, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Johannes ElvinDepartment of Molecular and Clinical Medicine - Nephrology, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Martin E JohanssonCenter for Molecular Pathology, Department of Laboratory Medicine, Lund University, SUS Malmö, Sweden.
Börje HaraldssonDepartment of Molecular and Clinical Medicine - Nephrology, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Jenny NyströmDepartment of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Lund University · SEUniversity of Gothenburg · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nephrotic syndrome, characterized by massive proteinuria, is caused by a large group of diseases including membranous nephropathy (MN) and focal segmental glomerulosclerosis (FSGS). Although the underlying mechanisms are beginning to unravel, therapy is unspecific and far from efficient. It has been suggested that adrenocorticotropic hormone (ACTH) has beneficial effects in patients with MN and possibly in other nephrotic diseases. We have previously reported that ACTH may act directly on podocytes through the melanocortin 1 receptor (MC1R). In the present study, we evaluate the effect of highly specific MC1R agonists in two different nephrotic disease models. Experimental MN: Passive Heymann nephritis (PHN) was induced in rats that were treated for four weeks with MS05, a selective MC1R agonist, or saline. The degree of albuminuria was significantly reduced over time and the effect was sustained one week after treatment withdrawal (p<0.05). Experimental FSGS: Based on a dose-response study, two doses of adriamycin were used for induction of nephropathy in Balb/c mice. Mice were treated with either a synthetic MC1R agonist (BMS-470539), with α-melanocyte stimulating hormone (α-MSH) or with saline. There was no beneficial effect of treatment. In summary, MC1R agonists reduce albuminuria and improve morphology in experimentally induced MN whereas they have no effect in experimental FSGS. The results illustrate the differences in these podocytopathies in terms of signaling mechanisms underlying proteinuria, and progression of disease.

Indexed as

AlbuminuriaAnimalsDisease Models, AnimalDoxorubicinGlomerulonephritis, MembranousGlomerulosclerosis, Focal SegmentalImidazolesMaleMiceMice, Inbred BALB CProteinuriaRatsRats, Sprague-DawleyReceptor, Melanocortin, Type 1BMS-470539DoxorubicinImidazolesReceptor, Melanocortin, Type 1

Identifiers

PMID24498203
PMCPMC3907561
OpenAlexW1971097484

What OpenQuestion holds

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Registered trials

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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.