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The Melanocortin-4 Receptor: Physiology, Pharmacology, and Pathophysiology
Open accessAbstract
The melanocortin-4 receptor (MC4R) was cloned in 1993 by degenerate PCR; however, its function was unknown. Subsequent studies suggest that the MC4R might be involved in regulating energy homeostasis. This hypothesis was confirmed in 1997 by a series of seminal studies in mice. In 1998, human genetic studies demonstrated that mutations in the MC4R gene can cause monogenic obesity. We now know that mutations in the MC4R are the most common monogenic form of obesity, with more than 150 distinct mutations reported thus far. This review will summarize the studies on the MC4R, from its cloning and tissue distribution to its physiological roles in regulating energy homeostasis, cachexia, cardiovascular function, glucose and lipid homeostasis, reproduction and sexual function, drug abuse, pain perception, brain inflammation, and anxiety. I will then review the studies on the pharmacology of the receptor, including ligand binding and receptor activation, signaling pathways, as well as its regulation. Finally, the pathophysiology of the MC4R in obesity pathogenesis will be reviewed. Functional studies of the mutant MC4Rs and the therapeutic implications, including small molecules in correcting binding and signaling defect, and their potential as pharmacological chaperones in rescuing intracellularly retained mutants, will be highlighted.
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In the citing paper
“Hyperphagia and increased adiposity lead to stimulation of POMC neurons and MC4R signalling, whereas energy deficits and weight loss reduce signalling in this pathway191,192.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [191]
In the citing paper
“In the ARC and brainstem, POMC-expressing neurons project to second-order neurons involved in BP regulation (for example, in the paraventricular nucleus (PVN)), where their axons release a-melanocyte-stimulating hormone (aMSH), the endogenous ligand for MC4R191 (FIG. 5a).”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [191]
In the citing paper
“The POMC-MC4R system is a major regulator of energy balance.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [191]
In the citing paper
“MC4R signals mainly through phosphorylation of cAMP and activation of protein kinase A (PKA)191.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [191]
In the citing paper
“The MC4R is a G protein-coupled 7 transmembrane receptor that increases cAMP phosphorylation and activates protein kinase A (PKA) [3, 26, 63]; therefore, blockade of these intracellular pathways attenuates MC4R actions [3, 63].”
From Role of the brain melanocortins in blood pressure regulation (2017) · cites this paper as [3]
In the citing paper
“The MC4R is a G protein-coupled 7 transmembrane receptor that increases cAMP phosphorylation and activates protein kinase A (PKA) [3, 26, 63]; therefore, blockade of these intracellular pathways attenuates MC4R actions [3, 63].”
From Role of the brain melanocortins in blood pressure regulation (2017) · cites this paper as [3]
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Metadata
- Authors
- Tao, Y.-X.
- Affiliations
- Auburn University (US)
- Corresponding author
- Tao, Ya-Xiong
- ORCID
- Tao, Ya-Xiong
- Venue
- Endocrine Reviews
- Publisher
- The Endocrine Society
- Published
- 2010-08-01
- Volume
- 31
- Issue
- 4
- Pages
- 506-543
- ISSN
- 0163-769X (ISSN-L)
- 1945-7189
- PMC
- PMC3365848
- OpenAlex
- W2120361515
- Cited by
- 531
- References
- 507
- Citations by year
- 2026: 25 · 2025: 32 · 2024: 34 · 2023: 34 · 2022: 31 · 2021: 41 · 2020: 41 · 2019: 33 · 2018: 29 · 2017: 32 · 2016: 21 · 2015: 29 · 2014: 39 · 2013: 47 · 2012: 30
- FWCI
- 16.04
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Endocrine Reviews (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R15DK077213)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Keywords
- melanocortin-4 receptor, energy homeostasis, monogenic obesity, MC4R mutations, cachexia, cardiovascular function, glucose homeostasis, lipid homeostasis, drug abuse, pain perception, neuroinflammation, anxiety, receptor pharmacology, ligand binding, receptor signaling pathways, pharmacological chaperones, obesity pathogenesis, small molecule drugs
- MeSH terms
- Amino Acid Sequence, Animals, Cachexia, Cardiovascular System, Cloning, Molecular, Energy Metabolism, Gene Expression Regulation, Glucose, Homeostasis, Humans, Molecular Sequence Data, Mutation, Obesity, Organ Specificity, Reproduction, Sexual Behavior, Signal Transduction, Sequence Alignment, Receptor, Melanocortin, Type 4, Lipid Metabolism
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