60 YEARS OF POMC: Adrenal and extra-adrenal functions of ACTH
Abstract
The pituitary adrenocorticotropic hormone (ACTH) plays a pivotal role in homeostasis and stress response and is thus the major component of the hypothalamo–pituitary–adrenal axis. After a brief summary of ACTH production from proopiomelanocortin (POMC) and on ACTH receptor properties, the first part of the review covers the role of ACTH in steroidogenesis and steroid secretion. We highlight the mechanisms explaining the differential acute vs chronic effects of ACTH on aldosterone and glucocorticoid secretion. The second part summarizes the effects of ACTH on adrenal growth, addressing its role as either a mitogenic or a differentiating factor. We then review the mechanisms involved in steroid secretion, from the classical Cyclic adenosine monophosphate second messenger system to various signaling cascades. We also consider how the interaction between the extracellular matrix and the cytoskeleton may trigger activation of signaling platforms potentially stimulating or repressing the steroidogenic potency of ACTH. Finally, we consider the extra-adrenal actions of ACTH, in particular its role in differentiation in a variety of cell types, in addition to its known lipolytic effects on adipocytes. In each section, we endeavor to correlate basic mechanisms of ACTH function with the pathological consequences of ACTH signaling deficiency and of overproduction of ACTH.
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Previously, direct receptor-mediated anti-inflammatory effects of ACTH and succinate on immune cells associated with blockages of pro-inflammatory polarization have been shown.
“Previously, the direct receptor-mediated anti-inflammatory effects of ACTH and succinate on immune cells associated with blockages of pro-inflammatory polarization have been shown [51,52,89].”
From Protective Effects of PGC-1α Activators on Ischemic Stroke in a Rat Model of Photochemically Induced Thrombosis (2021) · cites this paper as [51]
The drugs' abilities to exert neurotrophic effects may be mediated by activation of specific receptors: SUCNR1 for Mexidol and MCRs for Semax.
“The drugs’ abilities to exert neurotrophic effects may be mediated by the activation of specific receptors: SUCNR1 for Mexidol and receptors of the melanocortin family MCRs for Semax [51,52,59,60].”
From Protective Effects of PGC-1α Activators on Ischemic Stroke in a Rat Model of Photochemically Induced Thrombosis (2021) · cites this paper as [51]
Treatment with Mexidol and Semax, especially Mexidol, prolonged the period of PGC-1α activation, which may be related to receptor-mediated (by SUCNR1 and MCRs) initiation of calcium signaling cascades in neurons.
“The treatment with Mexidol and Semax, especially Mexidol, prolonged the period of PGC-1α activation, which may be related to the receptor-mediated (by SUCNR1 and MCRs) initiation of calcium signaling cascades in neurons [51,52,59,60].”
From Protective Effects of PGC-1α Activators on Ischemic Stroke in a Rat Model of Photochemically Induced Thrombosis (2021) · cites this paper as [51]
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- Authors
- Gallo-Payet, N.
- Affiliations
- 1Division of EndocrinologyDepartment of Medicine, Faculté de médecine et des sciences de la santé, Université de Sherbrooke, Sherbrooke, Quebec, Canada
- Venue
- Journal of Molecular Endocrinology
- Publisher
- Bioscientifica
- Published
- 2016-05
- Volume
- 56
- Issue
- 4
- Pages
- T135-T156
- ISSN
- 0952-5041 (ISSN-L)
- 1479-6813
- OpenAlex
- W2412941099
- Cited by
- 98
- References
- 227
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 9 · 2023: 11 · 2022: 5 · 2021: 16 · 2020: 9 · 2019: 9 · 2018: 7 · 2017: 14 · 2016: 8
- FWCI
- 1.85
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Molecular Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Université de Sherbrooke
- King's College London
- Canada Research Chairs
- Institute of Psychiatry, Psychology and Neuroscience, King’s College London
- Canadian Institutes of Health Research (MOP-10998)
- Faculty of Medicine and Health, University of Sydney
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal Regulation and Hypertension
- Keywords
- ACTH, proopiomelanocortin, ACTH receptor, hypothalamic-pituitary-adrenal axis, steroidogenesis, aldosterone secretion, glucocorticoid secretion, adrenal growth, cAMP signaling, extracellular matrix, cytoskeleton, cell differentiation, lipolysis, ACTH deficiency, ACTH excess, Cushing's disease
- MeSH terms
- Adrenal Cortex, Adrenal Cortex Hormones, Adrenal Glands, Adrenocorticotropic Hormone, Aldosterone, Animals, Cytoskeleton, Disease Susceptibility, Extracellular Matrix, Gene Expression Regulation, Humans, Periodicity, Protein Binding, Steroids, Signal Transduction, Reactive Oxygen Species, Adipocytes, MAP Kinase Signaling System, Genomics, Receptor, Melanocortin, Type 2
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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