Evidence map›Paper›PMID 24043794›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Urocortin 2 autocrine/paracrine and pharmacologic effects to activate AMP-activated protein kinase in the heart.

Ji Li, Dake Qi, Haiying Cheng, Xiaoyue Hu, Edward J Miller, Xiaohong Wu, Kerry S Russell, Nicole Mikush, Jiasheng Zhang, Lei Xiao and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.4field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Metabolic Association between Leptin and the Corticotropin Releasing Hormone.Endocrine, metabolic & immune disorders drug targets · 2019
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. The Modulation of Cardiac Contractile Function by the Pharmacological and Toxicological Effects of Urocortin2.Toxicological sciences : an official journal of the Society of Toxicology · 2015
    Article
  15. Article
  16. AMPK: energy sensor and survival mechanism in the ischemic heart.Trends in endocrinology and metabolism: TEM · 2015
    Review
  17. Review
  18. Article
  19. Article
  20. Autophagy, a process within reperfusion injury: an update.International journal of clinical and experimental pathology · 2014
    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

12 authors at 4 institutions in 1 country.

Ji LiDepartment of Pharmacology and Toxicology, University at Buffalo, The State University of New York, Buffalo, NY 14214.
Dake Qi
Haiying Cheng
Xiaoyue Hu
Edward J Miller
Xiaohong Wu
Kerry S Russell
Nicole Mikush
Jiasheng Zhang
Lei Xiao
Robert S Sherwin
Lawrence H Young
Yale University · USBoston University · USUniversity at Buffalo, State University of New York · USUniversity of Florida Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Urocortin 2 (Ucn2), a peptide of the corticotropin-releasing factor (CRF) family, binds with high affinity to type 2 CRF receptors (CRFR2) on cardiomyocytes and confers protection against ischemia/reperfusion. The mechanisms by which the Ucn2-CRFR2 axis mitigates against ischemia/reperfusion injury remain incompletely delineated. Activation of AMP-activated protein kinase (AMPK) also limits cardiac damage during ischemia/reperfusion. AMPK is classically activated by alterations in cellular energetics; however, hormones, cytokines, and additional autocrine/paracrine factors also modulate its activity. We examined the effects of both the endogenous cardiac Ucn2 autocrine/paracrine pathway and Ucn2 treatment on AMPK regulation. Ucn2 treatment increased AMPK activation and downstream acetyl-CoA carboxylase phosphorylation and glucose uptake in isolated heart muscles. These actions were blocked by the CRFR2 antagonist anti-sauvagine-30 and by a PKCε translocation-inhibitor peptide (εV1-2). Hypoxia-induced AMPK activation was also blunted in heart muscles by preincubation with either anti-sauvagine-30, a neutralizing anti-Ucn2 antibody, or εV1-2. Treatment with Ucn2 in vivo augmented ischemic AMPK activation and reduced myocardial injury and cardiac contractile dysfunction after regional ischemia/reperfusion in mice. Ucn2 also directly activated AMPK in ex vivo-perfused mouse hearts and diminished injury and contractile dysfunction during ischemia/reperfusion. Thus, both Ucn2 treatment and the endogenous cardiac Ucn2 autocrine/paracrine pathway activate AMPK signaling pathway, via a PKCε-dependent mechanism, defining a Ucn2-CRFR2-PKCε-AMPK pathway that mitigates against ischemia/reperfusion injury.

Indexed as

Acetyl-CoA CarboxylaseAMP-Activated Protein KinasesAnalysis of VarianceAnimalsAntibodies, NeutralizingCorticotropin-Releasing HormoneEnzyme ActivationImmunoblottingImmunohistochemistryMiceMyocardiumPeptide FragmentsPhosphorylationReceptors, Corticotropin-Releasing HormoneReperfusion InjurySignal TransductionAcetyl-CoA CarboxylaseAMP-Activated Protein KinasesAntibodies, Neutralizingantisauvagine 30Corticotropin-Releasing HormoneCRF receptor type 2Peptide FragmentsReceptors, Corticotropin-Releasing Hormoneurocortin 2, mouseUrocortinscardiac functionmetabolism

Identifiers

PMID24043794
PMCPMC3791748
OpenAlexW2076267095

What OpenQuestion holds

Textmetadata
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.