Linking vascular inflammation to obesity and atherosclerosis
Published 2014-05-06 · Original archive entry · Explore research explainers
A study in The Journal of Experimental Medicine shows that IκB kinase β (IKKβ) functions in smooth muscle cells to regulate vascular inflammatory responses and atherosclerosis development.
Inflammatory responses are the driving force of atherosclerosis, a process that involves the hardening and thickening of artery walls due to excess fatty deposits. IKKβ is a central coordinator of inflammatory responses that has been implicated in vascular diseases, but its role in atherosclerosis has been unclear.
Now, Changcheng Zhou and colleagues from the University of Kentucky show that deficiency of IKKβ in smooth muscle cells decreases vascular inflammation and atherosclerosis development in mice. Surprisingly, the lack of IKKβ also blocks the differentiation of fat cells and causes an accumulation of body fat precursor cells, thus protecting the animals from diet-induced obesity. These novel findings suggest that the kinase acts as a regulator of fat cell differentiation. The use of IKKβ inhibitors may therefore provide an innovative treatment for atherosclerosis, obesity, and metabolic disorders.
INFORMATION: Sui, Y., et al. 2014. J. Exp. Med. doi:10.1084/jem.20131281
About The Journal of Experimental Medicine The Journal of Experimental Medicine (JEM) is published by The Rockefeller University Press. All editorial decisions on manuscripts submitted are made by active scientists in conjunction with our in-house scientific editors. JEM content is posted to PubMed Central, where it is available to the public for free six months after publication. Authors retain copyright of their published works and third parties may reuse the content for non-commercial purposes under a creative commons license. For more information, please visit http://www.jem.org .
Research reported in the press release was supported by the National Insitutes of Health and the American Heart Association.
Inflammatory responses are the driving force of atherosclerosis, a process that involves the hardening and thickening of artery walls due to excess fatty deposits. IKKβ is a central coordinator of inflammatory responses that has been implicated in vascular diseases, but its role in atherosclerosis has been unclear.
Now, Changcheng Zhou and colleagues from the University of Kentucky show that deficiency of IKKβ in smooth muscle cells decreases vascular inflammation and atherosclerosis development in mice. Surprisingly, the lack of IKKβ also blocks the differentiation of fat cells and causes an accumulation of body fat precursor cells, thus protecting the animals from diet-induced obesity. These novel findings suggest that the kinase acts as a regulator of fat cell differentiation. The use of IKKβ inhibitors may therefore provide an innovative treatment for atherosclerosis, obesity, and metabolic disorders.
INFORMATION: Sui, Y., et al. 2014. J. Exp. Med. doi:10.1084/jem.20131281
About The Journal of Experimental Medicine The Journal of Experimental Medicine (JEM) is published by The Rockefeller University Press. All editorial decisions on manuscripts submitted are made by active scientists in conjunction with our in-house scientific editors. JEM content is posted to PubMed Central, where it is available to the public for free six months after publication. Authors retain copyright of their published works and third parties may reuse the content for non-commercial purposes under a creative commons license. For more information, please visit http://www.jem.org .
Research reported in the press release was supported by the National Insitutes of Health and the American Heart Association.