Evidence map›Paper›PMID 27489549›Full record

ReviewFrontiers in endocrinology2016

Role of ACTH in the Interactive/Paracrine Regulation of Adrenal Steroid Secretion in Physiological and Pathophysiological Conditions.

Hervé Lefebvre, Michaël Thomas, Céline Duparc, Jérôme Bertherat, Estelle Louiset

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 38 citations in OpenAlex.

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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

5 authors at 4 institutions in 1 country.

Hervé LefebvreU982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, INSERM, Institute for Research and Innovation in Biomedicine, Mont-Saint-Aignan, France; Normandie Université, UNIROUEN, Rouen, France; Department of Endocrinology, Diabetes and Metabolic Diseases, University Hospital of Rouen, Rouen, France.
Michaël ThomasU982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, INSERM, Institute for Research and Innovation in Biomedicine, Mont-Saint-Aignan, France; Normandie Université, UNIROUEN, Rouen, France.
Céline DuparcU982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, INSERM, Institute for Research and Innovation in Biomedicine, Mont-Saint-Aignan, France; Normandie Université, UNIROUEN, Rouen, France.
Jérôme BertheratU1016, INSERM, Institut Cochin, Paris, France; Department of Endocrinology and Metabolic Diseases, Hôpital Cochin, Assistance Publique-Hôpitaux de Paris, Paris, France.
Estelle LouisetU982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, INSERM, Institute for Research and Innovation in Biomedicine, Mont-Saint-Aignan, France; Normandie Université, UNIROUEN, Rouen, France.
Inserm · FRHôpital Cochin · FRNormandie Université · FRUniversité de Rouen Normandie · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the normal human adrenal gland, steroid secretion is regulated by a complex network of autocrine/paracrine interactions involving bioactive signals released by endothelial cells, nerve terminals, chromaffin cells, immunocompetent cells, and adrenocortical cells themselves. ACTH can be locally produced by medullary chromaffin cells and is, therefore, a major mediator of the corticomedullary functional interplay. Plasma ACTH also triggers the release of angiogenic and vasoactive agents from adrenocortical cells and adrenal mast cells and, thus, indirectly regulates steroid production through modulation of the adrenal blood flow. Adrenocortical neoplasms associated with steroid hypersecretion exhibit molecular and cellular defects that tend to reinforce the influence of paracrine regulatory loops on corticosteroidogenesis. Especially, ACTH has been found to be abnormally synthesized in bilateral macronodular adrenal hyperplasia responsible for hypercortisolism. In these tissues, ACTH is detected in a subpopulation of adrenocortical cells that express gonadal markers. This observation suggests that ectopic production of ACTH may result from impaired embryogenesis leading to abnormal maturation of the adrenogonadal primordium. Globally, the current literature indicates that ACTH is a major player in the autocrine/paracrine processes occurring in the adrenal gland in both physiological and pathological conditions.

Indexed as

ACTHadrenocortical cellsaldosteronealdosterone-producing adenomacortisolCushing’s syndromehyperplasiaVEGF

Identifiers

PMID27489549
PMCPMC4951519
OpenAlexW2481286122

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.