Evidence map›Paper›PMID 24602463›Full record

ReviewAdvances in chronic kidney disease2014

Leveraging melanocortin pathways to treat glomerular diseases.

Rujun Gong

Open access · bronzeAbstract readReview
In one paragraph

Review in Advances in chronic kidney disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. 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
  3. Article
  4. Intercepting the complement amplification loop through podocyte MC5R signaling ameliorates membranous nephropathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Synthetic ACTH for Treatment of Glomerular Diseases: A Case Series.Canadian journal of kidney health and disease · 2022
    Article
  14. Mechanisms of Scarring in Focal Segmental Glomerulosclerosis.Kidney diseases (Basel, Switzerland) · 2021
    Review
  15. IgA Nephropathy: An Interesting Autoimmune Kidney Disease.The American journal of the medical sciences · 2021
    Review
  16. Article
  17. Review
  18. Melanocortin 5 receptor signaling pathway in health and disease.Cellular and molecular life sciences : CMLS · 2020
    Review
  19. Article
  20. 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

1 author at 1 institution in 1 country.

Rujun GongDivision of Kidney Disease and Hypertension, Department of Medicine, Rhode Island Hospital, Brown University School of Medicine, Providence, RI. Electronic address: Rujun_Gong@Brown.edu.
Brown University · US

Funding

Therapeutic targeting of GSK3beta: A novel approach for podocyte protectionR01DK092485 · NIDDK · RHODE ISLAND HOSPITAL · PI GONG, RUJUN · 2011 to 2015
$1.8M
NIDDK NIH HHS R01 DK092485
6 · The paper itself

Abstract

The melanocortin system is a neuroimmunoendocrine hormone system that constitutes the fulcrum in the homeostatic control of a diverse array of physiological functions, including melanogenesis, inflammation, immunomodulation, adrenocortical steroidogenesis, hemodynamics, natriuresis, energy homeostasis, sexual function, and exocrine secretion. The kidney is a quintessential effector organ of the melanocortin hormone system with melanocortin receptors abundantly expressed by multiple kidney parenchymal cells, including podocytes, mesangial cells, glomerular endothelial cells, and renal tubular cells. Converging evidence unequivocally demonstrates that the melanocortin-based therapy using the melanocortin peptide adrenocorticotropic hormone (ACTH) is prominently effective in inducing remission of steroid-resistant nephrotic syndrome caused by various glomerular diseases, including membranous nephropathy, minimal change disease and focal segmental glomerulosclerosis, suggesting a steroidogenic-independent mechanism. Mechanistically, ACTH and other synthetic melanocortin analogues possess potent proteinuria-reducing and renoprotective activities that could be attributable to direct protection of glomerular cells and systemic immunomodulation. Thus, leveraging melanocortin signaling pathways using ACTH or novel synthetic melanocortin analogues represents a promising and pragmatic therapeutic strategy for glomerular diseases. This review article introduces the biophysiology of the melanocortin hormone system with an emphasis on the kidney as a target organ, discusses the existing data on melanocortin therapy for glomerular diseases, and elucidates the potential mechanisms of action.

Indexed as

Adrenocorticotropic Hormonealpha-MSHCosyntropinEndothelial CellsGlomerulonephritisGlomerulonephritis, MembranousGlomerulosclerosis, Focal SegmentalHormonesHumansKidneyKidney GlomerulusMelanocortinsMesangial CellsNephrosis, LipoidNephrotic SyndromePodocytesAdrenocorticotropic Hormoneadrenocorticotropin zincalpha-MSHCosyntropinHormonesMelanocortinsReceptors, MelanocortinAdrenocorticotropic hormoneGlomerulopathyMelanocortinNephrotic syndromePodocyte

Identifiers

PMID24602463
PMCPMC3950821
OpenAlexW2008367188

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.