Evidence map›Paper›PMID 35456013›Full record

ReviewCells2022

Research Status of the Orphan G Protein Coupled Receptor 158 and Future Perspectives.

Xianan Fu, Shoupeng Wei, Tao Wang, Hengxin Fan, Ying Zhang, Clive Da Costa, Sebastian Brandner, Guang Yang, Yihang Pan, Yulong He and 1 more

Abstract readReview
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Osteocalcin and GPR158: linking bone and brain function.Frontiers in cell and developmental biology · 2025
    Review
  3. Article
  4. Review
  5. Article
  6. The emerging roles of GPR158 in the regulation of the endocrine system.Frontiers in cell and developmental biology · 2022
    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

11 authors.

Xianan FuTomas Lindhal Nobel Laureate Laboratory, The Seventh Affiliated Hospital of Sun Yat-sen University (SYSU), No.628, Zhenyuan Rd., Guangming Dist., Shenzhen 518107, China.ORCID 0000-0001-9359-6314
Shoupeng WeiTomas Lindhal Nobel Laureate Laboratory, The Seventh Affiliated Hospital of Sun Yat-sen University (SYSU), No.628, Zhenyuan Rd., Guangming Dist., Shenzhen 518107, China.
Tao WangTomas Lindhal Nobel Laureate Laboratory, The Seventh Affiliated Hospital of Sun Yat-sen University (SYSU), No.628, Zhenyuan Rd., Guangming Dist., Shenzhen 518107, China.ORCID 0000-0002-2678-7521
Hengxin FanTomas Lindhal Nobel Laureate Laboratory, The Seventh Affiliated Hospital of Sun Yat-sen University (SYSU), No.628, Zhenyuan Rd., Guangming Dist., Shenzhen 518107, China.
Ying ZhangTomas Lindhal Nobel Laureate Laboratory, The Seventh Affiliated Hospital of Sun Yat-sen University (SYSU), No.628, Zhenyuan Rd., Guangming Dist., Shenzhen 518107, China.
Clive Da CostaThe Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.ORCID 0000-0002-0435-6747
Sebastian BrandnerDepartment of Neurodegenerative Disease, Institute of Neurology, University College London, Queen Square, London WC1N 3BG, UK.
Guang YangDepartment of Burn and Plastic Surgery, Institute of Translational Medicine, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Health Science Center, Shenzhen 518039, China.ORCID 0000-0001-5271-7079
Yihang PanTomas Lindhal Nobel Laureate Laboratory, The Seventh Affiliated Hospital of Sun Yat-sen University (SYSU), No.628, Zhenyuan Rd., Guangming Dist., Shenzhen 518107, China.
Yulong HeTomas Lindhal Nobel Laureate Laboratory, The Seventh Affiliated Hospital of Sun Yat-sen University (SYSU), No.628, Zhenyuan Rd., Guangming Dist., Shenzhen 518107, China.
Ningning LiTomas Lindhal Nobel Laureate Laboratory, The Seventh Affiliated Hospital of Sun Yat-sen University (SYSU), No.628, Zhenyuan Rd., Guangming Dist., Shenzhen 518107, China.ORCID 0000-0002-0414-5878

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

G-protein-coupled receptors (GPCRs) remain one of the most successful targets for therapeutic drugs approved by the US Food and Drug Administration (FDA). Many novel orphan GPCRs have been identified by human genome sequencing and considered as putative targets for refractory diseases. Of note, a series of studies have been carried out involving GPCR 158 (or GPR158) since its identification in 2005, predominantly focusing on the characterization of its roles in the progression of cancer and mental illness. However, advances towards an in-depth understanding of the biological mechanism(s) involved for clinical application of GPR158 are lacking. In this paper, we clarify the origin of the GPR158 evolution in different species and summarize the relationship between GPR158 and different diseases towards potential drug target identification, through an analysis of the sequences and substructures of GPR158. Further, we discuss how recent studies set about unraveling the fundamental features and principles, followed by future perspectives and thoughts, which may lead to prospective therapies involving GPR158.

Indexed as

Receptors, G-Protein-CoupledHumansUnited StatesReceptors, G-Protein-CoupledcancerGPCRGPR158psychological disorders

Identifiers

PMID35456013
PMCPMC9027133

What OpenQuestion holds

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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.