Visfatin/Nampt: An Adipokine with Cardiovascular Impact
Adipose tissue is acknowledged as an endocrine organ that releases bioactive factors termed adipokines. Visfatin was initially identified as a novel adipokine with insulin-mimetic properties in mice. This adipokine was identical to two previously described molecules, namely, pre-B cell colony-enhanc...
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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2013/946427 |
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| author | Tania Romacho Carlos F. Sánchez-Ferrer Concepción Peiró |
| author_facet | Tania Romacho Carlos F. Sánchez-Ferrer Concepción Peiró |
| author_sort | Tania Romacho |
| collection | DOAJ |
| description | Adipose tissue is acknowledged as an endocrine organ that releases bioactive factors termed adipokines. Visfatin was initially identified as a novel adipokine with insulin-mimetic properties in mice. This adipokine was identical to two previously described molecules, namely, pre-B cell colony-enhancing factor (PBEF) and the enzyme nicotinamide phosphoribosyltransferase (Nampt). Enhanced circulating visfatin/Nampt levels have been reported in metabolic diseases, such as obesity and type 2 diabetes. Moreover, visfatin/Nampt circulating levels correlate with markers of systemic inflammation. In cardiovascular diseases, visfatin/Nampt was initially proposed as a clinical marker of atherosclerosis, endothelial dysfunction, and vascular damage, with a potential prognostic value. Nevertheless, beyond being a surrogate clinical marker, visfatin/Nampt is an active player promoting vascular inflammation, and atherosclerosis. Visfatin/Nampt effects on cytokine and chemokine secretion, macrophage survival, leukocyte recruitment by endothelial cells, vascular smooth muscle inflammation and plaque destabilization make of this adipokine an active factor in the development and progression of atherosclerosis. Further research is required to fully understand the mechanisms mediating the cellular actions of this adipokine and to better characterize the factors regulating visfatin/Nampt expression and release in all these pathologic scenarios. Only then, we will be able to conclude whether visfatin/Nampt is a therapeutical target in cardiometabolic diseases. |
| format | Article |
| id | doaj-art-4cb744ea49974f97bf04a8e424c67ab3 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-4cb744ea49974f97bf04a8e424c67ab32025-02-03T01:24:31ZengWileyMediators of Inflammation0962-93511466-18612013-01-01201310.1155/2013/946427946427Visfatin/Nampt: An Adipokine with Cardiovascular ImpactTania Romacho0Carlos F. Sánchez-Ferrer1Concepción Peiró2Paul-Langerhans Group of Integrative Physiology, German Diabetes Center, Auf'm Hennekamp 65, 40225 Düsseldorf, GermanyDepartamento de Farmacología y Terapéutica, Facultad de Medicina, Universidad Autónoma de Madrid, Arzobispo Morcillo 4, 28029 Madrid, SpainDepartamento de Farmacología y Terapéutica, Facultad de Medicina, Universidad Autónoma de Madrid, Arzobispo Morcillo 4, 28029 Madrid, SpainAdipose tissue is acknowledged as an endocrine organ that releases bioactive factors termed adipokines. Visfatin was initially identified as a novel adipokine with insulin-mimetic properties in mice. This adipokine was identical to two previously described molecules, namely, pre-B cell colony-enhancing factor (PBEF) and the enzyme nicotinamide phosphoribosyltransferase (Nampt). Enhanced circulating visfatin/Nampt levels have been reported in metabolic diseases, such as obesity and type 2 diabetes. Moreover, visfatin/Nampt circulating levels correlate with markers of systemic inflammation. In cardiovascular diseases, visfatin/Nampt was initially proposed as a clinical marker of atherosclerosis, endothelial dysfunction, and vascular damage, with a potential prognostic value. Nevertheless, beyond being a surrogate clinical marker, visfatin/Nampt is an active player promoting vascular inflammation, and atherosclerosis. Visfatin/Nampt effects on cytokine and chemokine secretion, macrophage survival, leukocyte recruitment by endothelial cells, vascular smooth muscle inflammation and plaque destabilization make of this adipokine an active factor in the development and progression of atherosclerosis. Further research is required to fully understand the mechanisms mediating the cellular actions of this adipokine and to better characterize the factors regulating visfatin/Nampt expression and release in all these pathologic scenarios. Only then, we will be able to conclude whether visfatin/Nampt is a therapeutical target in cardiometabolic diseases.http://dx.doi.org/10.1155/2013/946427 |
| spellingShingle | Tania Romacho Carlos F. Sánchez-Ferrer Concepción Peiró Visfatin/Nampt: An Adipokine with Cardiovascular Impact Mediators of Inflammation |
| title | Visfatin/Nampt: An Adipokine with Cardiovascular Impact |
| title_full | Visfatin/Nampt: An Adipokine with Cardiovascular Impact |
| title_fullStr | Visfatin/Nampt: An Adipokine with Cardiovascular Impact |
| title_full_unstemmed | Visfatin/Nampt: An Adipokine with Cardiovascular Impact |
| title_short | Visfatin/Nampt: An Adipokine with Cardiovascular Impact |
| title_sort | visfatin nampt an adipokine with cardiovascular impact |
| url | http://dx.doi.org/10.1155/2013/946427 |
| work_keys_str_mv | AT taniaromacho visfatinnamptanadipokinewithcardiovascularimpact AT carlosfsanchezferrer visfatinnamptanadipokinewithcardiovascularimpact AT concepcionpeiro visfatinnamptanadipokinewithcardiovascularimpact |