Evidence map›Paper›PMID 23325074›Full record

ArticleKidney international2013

Adrenocorticotropic hormone ameliorates acute kidney injury by steroidogenic-dependent and -independent mechanisms.

Jin Si, Yan Ge, Shougang Zhuang, Li Juan Wang, Shan Chen, Rujun Gong

Open access · bronzeAbstract read
In one paragraph

Article in Kidney international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Interleukin-10 attenuates renal injury after myocardial infarction in diabetes.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2022
    Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Melanocortin 5 receptor signaling pathway in health and disease.Cellular and molecular life sciences : CMLS · 2020
    Review
  12. Review
  13. Article
  14. Review
  15. Renoprotective approaches and strategies in acute kidney injury.Pharmacology & therapeutics · 2016 · on this map
    Review
  16. Article
  17. Article
  18. Circadian Clocks, Stress, and Immunity.Frontiers in endocrinology · 2016
    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

6 authors at 3 institutions in 2 countries.

Jin SiDivision of Kidney Disease and Hypertension, Department of Medicine, Rhode Island Hospital, Brown Medical School, Providence, Rhode Island 02903, USA.
Yan Ge
Shougang Zhuang
Li Juan Wang
Shan Chen
Rujun Gong
Rhode Island Hospital · USArmy Medical University · CNProvidence College · 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 DK092485NIDDK NIH HHS R01DK092485
6 · The paper itself

Abstract

Adrenocorticotropic hormone (ACTH) has a renoprotective effect in chronic kidney disease; however, its effect on acute kidney injury (AKI) remains unknown. In a rat model of tumor necrosis factor (TNF)-induced AKI, we found that ACTH gel prevented kidney injury, corrected acute renal dysfunction, and improved survival. Morphologically, ACTH gel ameliorated TNF-induced acute tubular necrosis, associated with a reduction in tubular apoptosis. While the steroidogenic response to ACTH gel plateaued, the kidney-protective effect continued to increase at even higher doses, suggesting steroid-independent mechanisms. Of note, ACTH also acts as a key agonist of the melanocortin system, with its cognate melanocortin 1 receptor (MC1R) abundantly expressed in renal tubules. In TNF-injured tubular epithelial cells in vitro, ACTH reinstated cellular viability and eliminated apoptosis. This beneficial effect was blunted in MC1R-silenced cells, suggesting that this receptor mediates the anti-apoptotic signaling of ACTH. Moreover, ACTH gel protected mice against cecal ligation puncture-induced septic AKI better than α-melanocyte-stimulating hormone: a protein equal in biological activity to ACTH except for steroidogenesis. Thus, ACTH has additive renoprotective actions achieved by both steroid-dependent mechanisms and MC1R-directed anti-apoptosis. ACTH may represent a novel therapeutic strategy to prevent or treat AKI.

Indexed as

Acute Kidney InjuryAdrenocorticotropic HormoneAlbuminuriaAnimalsApoptosisCecumCells, CulturedCell SurvivalCorticosteroneCytoprotectionDisease Models, AnimalDose-Response Relationship, DrugGelsGlomerular Filtration RateKidneyKidney Tubular Necrosis, AcuteAdrenocorticotropic HormoneCorticosteroneGelsReceptor, Melanocortin, Type 1Tumor Necrosis Factor-alpha

Identifiers

PMID23325074
PMCPMC3612362
OpenAlexW2051190674

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.