ReviewEndocrine pathology2003
Why is the adrenal adrenergic?
Review in Endocrine pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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.
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.
Who cites it
17 citing papers in PubMed, 44 citations in OpenAlex.
- Voluntary activation of the sympathetic nervous system and attenuation of the innate immune response in humans.Proceedings of the National Academy of Sciences of the United States of America · 2014Trial
- Spatial transcriptomics exploration of the primary neuroblastoma microenvironment in archived FFPE samples unveils novel paracrine interactions.The Journal of pathology · 2025Article
- Tumor metabolism in pheochromocytomas: clinical and therapeutic implications.Exploration of targeted anti-tumor therapy · 2024Review
- Domestication of farmed fishFrontiers in endocrinology · 2022Review
- The abnormalities of adrenomedullary hormonal system in genetic hypertension: Their contribution to altered regulation of blood pressure.Physiological research · 2021Review
- Review
- Human nicotinic receptors in chromaffin cells: characterization and pharmacology.Pflugers Archiv : European journal of physiology · 2018Review
- Adrenal Gland Microenvironment and Its Involvement in the Regulation of Stress-Induced Hormone Secretion during Sepsis.Frontiers in endocrinology · 2016Review
- Urinary bladder paraganglioma presenting as micturition-induced palpitations, dyspnea, and angina.The American journal of case reports · 2015Article
- Catecholamine metabolism in paraganglioma and pheochromocytoma: similar tumors in different sites?PloS one · 2015Article
- Pannexin 1 channels: new actors in the regulation of catecholamine release from adrenal chromaffin cells.Frontiers in cellular neuroscience · 2014Article
- The LIM-Homeodomain transcription factor Islet-1 is required for the development of sympathetic neurons and adrenal chromaffin cells.Developmental biology · 2013Article
- Role of reactive oxygen species in the neural and hormonal regulation of the PNMT gene in PC12 cells.Oxidative medicine and cellular longevity · 2011Article
- Review: the role of neural crest cells in the endocrine system.Endocrine pathology · 2009Review
- Adrenergic differentiation and Ret expression in rat pheochromocytomas.Endocrine pathology · 2008Article
- Different expression of catecholamine transporters in phaeochromocytomas from patients with von Hippel-Lindau syndrome and multiple endocrine neoplasia type 2.European journal of endocrinology · 2005Article
- Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The adrenal gland is the body's primary source for epinephrine production and release, and the chromaffin cells that comprise the adrenal medulla possess all of the catecholamine biosynthetic machinery, including phenylethanolamine N-methyltransferase (PNMT), the enzyme synthesizing epinephrine from norepinephrine. In most species, epinephrine, also known as adrenaline, is the predominant neurotransmitter/neurohormone expressed by chromaffin cells. Present knowledge about "what makes the adrenal adrenergic" is derived from studies of normal and neoplastic adrenal medullary tissue and cells, with the PNMT gene serving as a marker of adrenergic function. The preference for adrenergic expression occurs, in part, because of the juxtaposition of adrenal medulla and adrenal cortex, as the cortex provides high circulating levels of glucocorticoids to the medulla. However, although glucocorticoids and the activated glucocorticoid receptor clearly are critical elements, they are apparently not the sole components defining the adrenergic phenotype. Other factors may include several transcriptional activators of the PNMT gene: Egr-1, AP2, Sp1, and MAZ. The existence of transcription factors that silence PNMT expression in noradrenergic cells has also been postulated. Understanding the requirements for adrenergic expression may provide important insights and potential therapies for disorders in which adrenergic/catecholaminergic dysfunction leads to illnesses refractory to present treatment strategies.
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Registered trials
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.