Evidence map›Paper›PMID 31261897›Full record

ReviewInternational journal of molecular sciences2019

Potential Utility of Biased GPCR Signaling for Treatment of Psychiatric Disorders.

Hidetoshi Komatsu, Mamoru Fukuchi, Yugo Habata

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

14 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  5. α-Arrestins and Their Functions: From Yeast to Human Health.International journal of molecular sciences · 2022
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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

3 authors at 3 institutions in 1 country.

Hidetoshi KomatsuMedical Affairs, Kyowa Pharmaceutical Industry Co., Ltd. (A Lupin Group Company), Osaka 530-0005, Japan. hidetkomatsu@fuji.waseda.jp.
Mamoru FukuchiLaboratory of Molecular Neuroscience, Faculty of Pharmacy, Takasaki University of Health and Welfare, Gunma 370-0033, Japan.
Yugo HabataDepartment of Food & Nutrition, Yamanashi Gakuin Junior College, Kofu 400-8575, Japan.
Nagoya University · JPTakasaki University of Health and Welfare · JPYamanashi Gakuin University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tremendous advances have been made recently in the identification of genes and signaling pathways associated with the risks for psychiatric disorders such as schizophrenia and bipolar disorder. However, there has been a marked reduction in the pipeline for the development of new psychiatric drugs worldwide, mainly due to the complex causes that underlie these disorders. G-protein coupled receptors (GPCRs) are the most common targets of antipsychotics such as quetiapine and aripiprazole, and play pivotal roles in controlling brain function by regulating multiple downstream signaling pathways. Progress in our understanding of GPCR signaling has opened new possibilities for selective drug development. A key finding has been provided by the concept of biased ligands, which modulate some, but not all, of a given receptor's downstream signaling pathways. Application of this concept raises the possibility that the biased ligands can provide therapeutically desirable outcomes with fewer side effects. Instead, this application will require a detailed understanding of the mode of action of antipsychotics that drive distinct pharmacologies. We review our current understanding of the mechanistic bases for multiple signaling modes by antipsychotics and the potential of the biased modulators to treat mental disorders.

Indexed as

Signal TransductionAnimalsAntipsychotic AgentsDopamine D2 Receptor AntagonistsHumansMental DisordersReceptors, Dopamine D2Antipsychotic AgentsDopamine D2 Receptor AntagonistsReceptors, Dopamine D2aripiprazolebiased ligandbipolar disorderdopamine D2 receptorGPCRpsychiatric disorderquetiapineschizophreniaβ-arrestin

Identifiers

PMID31261897
PMCPMC6651563
OpenAlexW2955386396

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.