GPR109A and Vascular Inflammation
GPR109A has generated expanding interest since its discovery as the receptor for niacin a decade ago, along with deorphanisation as the receptor for endogenous ligand 3-hydroxy-butyrate shortly after. This interest is generated especially because of the continuing exploration of niacin's "...
| Հիմնական հեղինակներ: | , , |
|---|---|
| Ձևաչափ: | Journal article |
| Լեզու: | English |
| Հրապարակվել է: |
2013
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| _version_ | 1826256470107226112 |
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| author | Chai, J Digby, J Choudhury, R |
| author_facet | Chai, J Digby, J Choudhury, R |
| author_sort | Chai, J |
| collection | OXFORD |
| description | GPR109A has generated expanding interest since its discovery as the receptor for niacin a decade ago, along with deorphanisation as the receptor for endogenous ligand 3-hydroxy-butyrate shortly after. This interest is generated especially because of the continuing exploration of niacin's "pleiotropic" mechanisms of action and its potential in the "cross-talk" between metabolic and inflammatory pathways. As GPR109A's primary pharmacological ligand in clinical use, niacin has been used for over 50 years in the treatment of cardiovascular disease, mainly due to its favourable effects on plasma lipoproteins. However, it has become apparent that niacin also possesses lipoprotein-independent effects that influence inflammatory pathways mediated through GPR109A. In addition to its G-protein-mediated effects, recent evidence has emerged to support alternative GPR109A signalling via adaptive protein β-arrestins. In this article, we consider the role of GPR109A and its downstream effects in the context of atherosclerosis and vascular inflammation, along with insights into strategy for future drug development. © 2013 The Author(s). |
| first_indexed | 2024-03-06T18:02:45Z |
| format | Journal article |
| id | oxford-uuid:006007a5-86b7-46fb-ba54-37e5a23cf80d |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-06T18:02:45Z |
| publishDate | 2013 |
| record_format | dspace |
| spelling | oxford-uuid:006007a5-86b7-46fb-ba54-37e5a23cf80d2022-03-26T08:29:12ZGPR109A and Vascular InflammationJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:006007a5-86b7-46fb-ba54-37e5a23cf80dEnglishSymplectic Elements at Oxford2013Chai, JDigby, JChoudhury, RGPR109A has generated expanding interest since its discovery as the receptor for niacin a decade ago, along with deorphanisation as the receptor for endogenous ligand 3-hydroxy-butyrate shortly after. This interest is generated especially because of the continuing exploration of niacin's "pleiotropic" mechanisms of action and its potential in the "cross-talk" between metabolic and inflammatory pathways. As GPR109A's primary pharmacological ligand in clinical use, niacin has been used for over 50 years in the treatment of cardiovascular disease, mainly due to its favourable effects on plasma lipoproteins. However, it has become apparent that niacin also possesses lipoprotein-independent effects that influence inflammatory pathways mediated through GPR109A. In addition to its G-protein-mediated effects, recent evidence has emerged to support alternative GPR109A signalling via adaptive protein β-arrestins. In this article, we consider the role of GPR109A and its downstream effects in the context of atherosclerosis and vascular inflammation, along with insights into strategy for future drug development. © 2013 The Author(s). |
| spellingShingle | Chai, J Digby, J Choudhury, R GPR109A and Vascular Inflammation |
| title | GPR109A and Vascular Inflammation |
| title_full | GPR109A and Vascular Inflammation |
| title_fullStr | GPR109A and Vascular Inflammation |
| title_full_unstemmed | GPR109A and Vascular Inflammation |
| title_short | GPR109A and Vascular Inflammation |
| title_sort | gpr109a and vascular inflammation |
| work_keys_str_mv | AT chaij gpr109aandvascularinflammation AT digbyj gpr109aandvascularinflammation AT choudhuryr gpr109aandvascularinflammation |