Evidence map›Paper›PMID 25489106›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Antagonist of GH-releasing hormone receptors alleviates experimental ocular inflammation.

Yong Jie Qin, Sun On Chan, Kelvin Kam Lung Chong, Benjamin Fuk Loi Li, Tsz Kin Ng, Yolanda Wong Ying Yip, Haoyu Chen, Mingzhi Zhang, Norman L Block, Herman S Cheung 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, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Growth hormone-releasing hormone and cancer.Reviews in endocrine & metabolic disorders · 2025
    Review
  8. Growth hormone - releasing hormone in the immune system.Reviews in endocrine & metabolic disorders · 2025
    Review
  9. Growth hormone-releasing hormone receptor (GHRH-R) and its signaling.Reviews in endocrine & metabolic disorders · 2025
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Growth Hormone, Not IGF-1 Is the Key Longevity Regulator in Mammals.The journals of gerontology. Series A, Biological sciences and medical sciences · 2022
    Article
  20. Article
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 2 institutions in 3 countries.

Yong Jie QinDepartment of Ophthalmology & Visual Sciences and.
Sun On ChanSchool of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong;
Kelvin Kam Lung ChongDepartment of Ophthalmology & Visual Sciences and Joint Shantou International Eye Center, Shantou University and The Chinese University of Hong Kong, 515041 Shantou, China;
Benjamin Fuk Loi LiDepartment of Ophthalmology & Visual Sciences and.
Tsz Kin NgDepartment of Ophthalmology & Visual Sciences and Joint Shantou International Eye Center, Shantou University and The Chinese University of Hong Kong, 515041 Shantou, China;
Yolanda Wong Ying YipDepartment of Ophthalmology & Visual Sciences and.
Haoyu ChenJoint Shantou International Eye Center, Shantou University and The Chinese University of Hong Kong, 515041 Shantou, China;
Mingzhi ZhangJoint Shantou International Eye Center, Shantou University and The Chinese University of Hong Kong, 515041 Shantou, China;
Norman L BlockDepartment of Biomedical Engineering, University of Miami, Coral Gables, FL 33146; Endocrine, Polypeptide, and Cancer Institute, South Florida Veterans Affairs Foundation for Research and Education, and Department of Pathology and Divisions of Hematology and Oncology and Endocrinology, Department of Medicine, Miller School of Medicine, University of Miami, Miami, FL 33136.
Herman S CheungDepartment of Biomedical Engineering, University of Miami, Coral Gables, FL 33146; Geriatric Research, Education and Clinical Center, Veterans Affairs Medical Center, Miami, FL 33125; and.
Andrew V SchallyEndocrine, Polypeptide, and Cancer Institute, South Florida Veterans Affairs Foundation for Research and Education, and Department of Pathology and Divisions of Hematology and Oncology and Endocrinology, Department of Medicine, Miller School of Medicine, University of Miami, Miami, FL 33136 andrew.schally@va.gov cppang@cuhk.edu.hk.
Chi Pui PangDepartment of Ophthalmology & Visual Sciences and Joint Shantou International Eye Center, Shantou University and The Chinese University of Hong Kong, 515041 Shantou, China; andrew.schally@va.gov cppang@cuhk.edu.hk.
Chinese University of Hong Kong · CNUniversity of Miami · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disruptions in immunity and occurrence of inflammation cause many eye diseases. The growth hormone-releasing hormone-growth hormone-insulin-like growth factor-1 (GHRH-GH-IGF1) axis exerts regulatory effects on the immune system. Its involvement in ocular inflammation remains to be investigated. Here we studied this signaling in endotoxin-induced uveitis (EIU) generated by LPS. The increase in GHRH receptor (GHRH-R) protein levels was parallel to the increase in mRNA levels of pituitary-specific transcription factor-1, GHRH-R splice variant 1, GHRH, and GH following LPS insult. Elevation of GHRH-R and GH receptor was localized on the epithelium of the iris and ciliary body, and GHRH-R was confined to the infiltrating macrophages and leukocytes in aqueous humor but not to those in stroma. Treatment with GHRH-R antagonist decreased LPS-stimulated surges of GH and IGF1 in aqueous humor and alleviated inflammation by reducing the infiltration of macrophages and leukocytes and the production of TNF-α, IL-1β, and monocyte chemotactic protein-1. Our results indicate that inflammation in the iris and ciliary body involves the activation of GHRH signaling, which affects the recruitment of immune cells and the production of proinflammatory mediators that contribute to EIU pathogenesis. Moreover, the results suggest that GHRH-R antagonists are potential therapeutic agents for the treatment of acute ocular inflammation.

Indexed as

AnimalsEnzyme-Linked Immunosorbent AssayGrowth HormoneGrowth Hormone-Releasing HormoneInsulin-Like Growth Factor IRatsRats, Sprague-DawleyReceptors, NeuropeptideReceptors, Pituitary Hormone-Regulating HormoneSermorelinUveitisGHRH(1-29)NH2, (PhAc-Ada)(0)-Tyr(1), Arg(2), Fpa(5,6), Ala(8), Har(9), Tyr(Me)(10), His(11), Orn(12,) Abu(15), His(20), Orn(21), Nle(27), Arg(28), Har(29)-Growth HormoneGrowth Hormone-Releasing HormoneInsulin-Like Growth Factor IReceptors, NeuropeptideReceptors, Pituitary Hormone-Regulating HormoneSermorelinsomatotropin releasing hormone receptorexperimental uveitisGHRH analogsGHRH–GH–IGF1 axis

Identifiers

PMID25489106
PMCPMC4280596
OpenAlexW2008213207

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.