Evidence map›Paper›PMID 33266265›Full record

ReviewInternational journal of molecular sciences2020

The Mechanisms Underlying Autonomous Adrenocorticotropic Hormone Secretion in Cushing's Disease.

Hidenori Fukuoka, Hiroki Shichi, Masaaki Yamamoto, Yutaka Takahashi

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Cushing syndrome.Nature reviews. Disease primers · 2025
    Review
  7. Review
  8. Hypothalamic-Pituitary-Adrenal Axis and Epilepsy.Journal of clinical neurology (Seoul, Korea) · 2024
    Review
  9. Review
  10. Article
  11. Dexamethasone suppression forCancer imaging : the official publication of the International Cancer Imaging Society · 2023
    Article
  12. Review
  13. Article
  14. Gene Mutations in Cushing's Syndrome.Molecular syndromology · 2023
    Review
  15. Article
  16. Article
  17. Genetic Basis of ACTH-Secreting Adenomas.International journal of molecular sciences · 2022
    Review
  18. Article
  19. Pathophysiology of Mild Hypercortisolism: From the Bench to the Bedside.International journal of molecular sciences · 2022
    Review
  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

4 authors at 3 institutions in 1 country.

Hidenori FukuokaDivision of Diabetes and Endocrinology, Kobe University Hospital, 7-5-2, Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.ORCID 0000-0001-9255-653X
Hiroki ShichiDivision of Diabetes and Endocrinology, Kobe University Graduate School of Medicine, 7-5-2, Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.
Masaaki YamamotoDivision of Diabetes and Endocrinology, Kobe University Hospital, 7-5-2, Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.
Yutaka TakahashiDivision of Diabetes and Endocrinology, Kobe University Graduate School of Medicine, 7-5-2, Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.
Kobe University Hospital · JPKobe University · JPNara Medical University · JP

Funding

Grant-in-Aid for Scientific Research from the Japanese Ministry of Education, Culture, Sports, Science and Technology 19K09003
6 · The paper itself

Abstract

Cushing's disease caused due to adrenocorticotropic hormone (ACTH)-secreting pituitary adenomas (ACTHomas) leads to hypercortisolemia, resulting in increased morbidity and mortality. Autonomous ACTH secretion is attributed to the impaired glucocorticoid negative feedback (glucocorticoid resistance) response. Interestingly, other conditions, such as ectopic ACTH syndrome (EAS) and non-neoplastic hypercortisolemia (NNH, also known as pseudo-Cushing's syndrome) also exhibit glucocorticoid resistance. Therefore, to differentiate between these conditions, several dynamic tests, including those with desmopressin (DDAVP), corticotrophin-releasing hormone (CRH), and Dex/CRH have been developed. In normal pituitary corticotrophs, ACTH synthesis and secretion are regulated mainly by CRH and glucocorticoids, which are the ACTH secretion-stimulating and -suppressing factors, respectively. These factors regulate ACTH synthesis and secretion through genomic and non-genomic mechanisms. Conversely, glucocorticoid negative feedback is impaired in ACTHomas, which could be due to the overexpression of 11β-HSD2, HSP90, or TR4, or loss of expression of CABLES1 or nuclear BRG1 proteins. Genetic analysis has indicated the involvement of several genes in the etiology of ACTHomas, including

Indexed as

Disease SusceptibilityACTH-Secreting Pituitary AdenomaACTH Syndrome, EctopicAdrenocorticotropic HormoneBiomarkersCushing SyndromeDiagnosis, DifferentialFemaleGene Expression RegulationGlucocorticoidsHumansMaleSignal TransductionAdrenocorticotropic HormoneBiomarkersGlucocorticoidsadrenocorticotrophic hormoneCushing’s diseaseectopic ACTH syndromeglucocorticoid resistance

Identifiers

PMID33266265
PMCPMC7730156
OpenAlexW3110223746

What Socratic 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 Socratic graph.