Evidence map›Paper›PMID 16052036›Full record

ReviewNeuromolecular medicine2005

Class II G protein-coupled receptors and their ligands in neuronal function and protection.

Bronwen Martin, Rakel Lopez de Maturana, Randall Brenneman, Tom Walent, Mark P Mattson, Stuart Maudsley

Abstract readReview
In one paragraph

Review in Neuromolecular medicine, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
0.9field-weighted citation impact, top 33% 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

47 citing papers in PubMed, 92 citations in OpenAlex.

  1. Article
  2. Article
  3. The role of GIPR in food intake control.Frontiers in endocrinology · 2025
    Review
  4. Review
  5. Article
  6. Intestinal Enteroendocrine Cells: Present and Future Druggable Targets.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Article
  9. Review
  10. The Relaxin-3 Receptor, RXFP3, Is a Modulator of Aging-Related Disease.International journal of molecular sciences · 2022
    Review
  11. Review
  12. Article
  13. Agonistic analog of growth hormone-releasing hormone promotes neurofunctional recovery and neural regeneration in ischemic stroke.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  14. Article
  15. Peptide-Liganded G Protein-Coupled Receptors as Neurotherapeutics.ACS pharmacology & translational science · 2020
    Review
  16. Article
  17. Article
  18. Article
  19. Phosphodiesterase Inhibitors Revert Axonal Dystrophy in Friedreich's Ataxia Mouse Model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019
    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 2 institutions in 2 countries.

Bronwen MartinLaboratory of Neurosciences, National Institute on Ageing Intramural Research Program, Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA.
Rakel Lopez de Maturana
Randall Brenneman
Tom Walent
Mark P Mattson
Stuart Maudsley
National Institute on Aging · USQueens University · BD

Funding

Age and pathology-induced alteration of G protein-coupled receptor signalingZ01AG000318 · NIA · NATIONAL INSTITUTE ON AGING · PI MAUDSLEY, STUART · 2007 to 2008
$905k
Intramural NIH HHS Z01 AG000318
6 · The paper itself

Abstract

G protein-coupled receptors (GPCRs) play pivotal roles in regulating the function and plasticity of neuronal circuits in the nervous system. Among the myriad of GPCRs expressed in neural cells, class II GPCRs which couples predominantly to the Gs-adenylate cyclase-cAMP signaling pathway, have recently received considerable attention for their involvement in regulating neuronal survival. Neuropeptides that activate class II GPCRs include secretin, glucagon-like peptides (GLP-1 and GLP-2), growth hormone-releasing hormone (GHRH), pituitary adenylate cyclase activating peptide (PACAP), corticotropin-releasing hormone (CRH), vasoactive intestinal peptide (VIP), parathyroid hormone (PTH), and calcitonin-related peptides. Studies of patients and animal and cell culture models, have revealed possible roles for class II GPCRs signaling in the pathogenesis of several prominent neurodegenerative conditions including stroke, Alzheimer's, Parkinson's, and Huntington's diseases. Many of the peptides that activate class II GPCRs promote neuron survival by increasing the resistance of the cells to oxidative, metabolic, and excitotoxic injury. A better understanding of the cellular and molecular mechanisms by which class II GPCRs signaling modulates neuronal survival and plasticity will likely lead to novel therapeutic interventions for neurodegenerative disorders.

Indexed as

AnimalsCell SurvivalCentral Nervous SystemCytoprotectionHumansLigandsNeurodegenerative DiseasesNeuronsNeuropeptidesOxidative StressReceptors, G-Protein-CoupledSignal TransductionLigandsNeuropeptidesReceptors, G-Protein-Coupled

Identifiers

PMID16052036
PMCPMC2636744
OpenAlexW1991739750

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.