The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Serotonin receptors and heart valve disease—It was meant 2B
Open accessAbstract
Carcinoid heart disease was one of the first valvular pathologies studied in molecular detail, and early research identified serotonin produced by oncogenic enterochromaffin cells as the likely culprit in causing changes in heart valve tissue. Researchers and physicians in the mid-1960s noted a connection between the use of several ergot-derived medications with structures similar to serotonin and the development of heart valve pathologies similar to those observed in carcinoid patients. The exact serotonergic target that mediated valvular pathogenesis remained a mystery for many years until similar cases were reported in patients using the popular diet drug Fen-Phen in the late 1990s. The Fen-Phen episode sparked renewed interest in serotonin-mediated valve disease, and studies led to the identification of the 5-HT2B receptor as the likely molecular target leading to heart valve tissue fibrosis. Subsequent studies have identified numerous other activators of the 5-HT2B receptor, and consequently, the use of many of these molecules has been linked to heart valve disease. Herein, we: review the molecular properties of the 5-HT2B receptor including factors that differentiate the 5-HT2B receptor from other 5-HT receptor subtypes, discuss the studies that led to the identification of the 5-HT2B receptor as the mediator of heart valve disease, present current efforts to identify potential valvulopathogens by screening for 5-HT2B receptor activity, and speculate on potential therapeutic benefits of 5-HT2B receptor targeting.
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Cites
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Drugs and Valvular Heart Disease
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“…the NIMH Psychoactive Drug Screening Program has sought to screen large numbers of FDA-approved drugs and drug-like compounds for agonist activity at 5-HT2B receptors in order to identify drugs/chemotypes with HVD liability (Setola, Dukat et al. 2005; Roth 2007; Huang, Setola et al. 2009).”
BackgroundMethodInfluentialSelf-citationStrategies to Discover Unexpected Targets for Drugs Active at G Protein–Coupled Receptors
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Self-citation
Cited by
Polypharmacology – Foe or Friend?
Peters, J.-U. (2013) · Journal of Medicinal Chemistry · doi:10.1021/jm400856t · Cited by 465
AGA Clinical Practice Guideline on Pharmacological Interventions for Adults With Obesity
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Psychedelics in Psychiatry: Neuroplastic, Immunomodulatory, and Neurotransmitter Mechanisms
Inserra, A., De Gregorio, D., & Gobbi, G. (2021) · Pharmacological Reviews · doi:10.1124/pharmrev.120.000056 · Cited by 232
Mabry, K. M., Payne, S. Z., & Anseth, K. S. (2016) · Biomaterials · doi:10.1016/j.biomaterials.2015.09.035 · Cited by 124
Complications from carcinoid syndrome: Review of the current evidence
Mota, J. M., Sousa, L. G., & Riechelmann, R. P. (2016) · ecancermedicalscience · doi:10.3332/ecancer.2016.662 · Cited by 99
Metadata
- Authors
- Hutcheson, J. D., Setola, V., Roth, B. L., & Merryman, W. D.
- Venue
- Pharmacology & Therapeutics
- Publisher
- Elsevier BV
- Published
- 2011-11
- Volume
- 132
- Issue
- 2
- Pages
- 146-157
- ISSN
- 0163-7258 (ISSN-L)
- OpenAlex
- W2085050037
- Cited by
- 252
- References
- 9
- FWCI
- 9.23
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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