Evidence map›Paper›PMID 33096674›Full record

ReviewCells2020

Growth Hormone-Releasing Hormone in Lung Physiology and Pulmonary Disease.

Chongxu Zhang, Tengjiao Cui, Renzhi Cai, Medhi Wangpaichitr, Mehdi Mirsaeidi, Andrew V Schally, Robert M Jackson

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Single-cell dissection of pleural and systemic immunity uncovers pathogen-specific immune reprogramming in tuberculosis versus lung adenocarcinoma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  5. Review
  6. Review
  7. Article
  8. Growth hormone-releasing hormone and cancer.Reviews in endocrine & metabolic disorders · 2025
    Review
  9. Review
  10. Article
  11. Review
  12. Advancements in lung regeneration: from bench to bedside.Journal of translational medicine · 2025
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Alleviation of LPS-induced Endothelial Injury due to GHRH Antagonist Treatment.International journal of peptide research and therapeutics · 2024
    Article
  18. Article
  19. 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

7 authors at 2 institutions in 1 country.

Chongxu ZhangResearch Service, Miami VAHS, Miami, FL 33125, USA.
Tengjiao CuiResearch Service, Miami VAHS, Miami, FL 33125, USA.
Renzhi CaiResearch Service, Miami VAHS, Miami, FL 33125, USA.
Medhi WangpaichitrResearch Service, Miami VAHS, Miami, FL 33125, USA.
Mehdi MirsaeidiResearch Service, Miami VAHS, Miami, FL 33125, USA.ORCID 0000-0001-5298-8442
Andrew V SchallyResearch Service, Miami VAHS, Miami, FL 33125, USA.
Robert M JacksonResearch Service, Miami VAHS, Miami, FL 33125, USA.ORCID 0000-0001-5892-1193
Miami VA Healthcare System · USUniversity of Miami · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growth hormone-releasing hormone (GHRH) is secreted primarily from the hypothalamus, but other tissues, including the lungs, produce it locally. GHRH stimulates the release and secretion of growth hormone (GH) by the pituitary and regulates the production of GH and hepatic insulin-like growth factor-1 (IGF-1). Pituitary-type GHRH-receptors (GHRH-R) are expressed in human lungs, indicating that GHRH or GH could participate in lung development, growth, and repair. GHRH-R antagonists (i.e., synthetic peptides), which we have tested in various models, exert growth-inhibitory effects in lung cancer cells in vitro and in vivo in addition to having anti-inflammatory, anti-oxidative, and pro-apoptotic effects. One antagonist of the GHRH-R used in recent studies reviewed here, MIA-602, lessens both inflammation and fibrosis in a mouse model of bleomycin lung injury. GHRH and its peptide agonists regulate the proliferation of fibroblasts through the modulation of extracellular signal-regulated kinase (ERK) and Akt pathways. In addition to downregulating GH and IGF-1, GHRH-R antagonist MIA-602 inhibits signaling pathways relevant to inflammation, including p21-activated kinase 1-signal transducer and activator of transcription 3/nuclear factor-kappa B (PAK1-STAT3/NF-κB and ERK). MIA-602 induces fibroblast apoptosis in a dose-dependent manner, which is an effect that is likely important in antifibrotic actions. Taken together, the novel data reviewed here show that GHRH is an important peptide that participates in lung homeostasis, inflammation, wound healing, and cancer; and GHRH-R antagonists may have therapeutic potential in lung diseases.

Indexed as

AnimalsCell RespirationGrowth Hormone-Releasing HormoneHumansLungLung DiseasesOxidative StressSignal TransductionGrowth Hormone-Releasing Hormoneantagonistsbleomycingrowth hormone-releasing hormoneidiopathic pulmonary fibrosis

Identifiers

PMID33096674
PMCPMC7589146
OpenAlexW3094027664

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.