Visceral adipose tissue is a primary site of chronic inflammation in obesity and may contribute to systemic inflammation and development of atherosclerotic vascular disease. Few studies identify molecular mechanisms and secretory pathways which mediate this process. In this edition of Clinical Science, Kwok et al. utilize a transgenic mouse in which dominant-negative c-Jun NH2 terminal kinase (dnJNK) expression is restricted to adipose tissue to implicate JNK-driven expression of adipocyte fatty acid binding protein (A-FABP) in visceral adipose tissue as a key secretory pathway to exacerbate development of atherosclerosis in ApoE-/- mice. They further demonstrate that ApoE-/- mice transplanted with visceral adipose tissue in which JNK has been inactivated display less systemic inflammation and develop significantly less atherosclerosis compared with control mice. Together, the findings of the present study reinforce our understanding of visceral adipose tissue as a secretory organ and the importance of the JNK/A-FABP pathway in mediating adipose vascular cross-talk and exacerbation of atherosclerosis.
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Commentary| October 11 2016
Adipose inflammation at the heart of vascular disease
Michael V. Autieri
*Department of Physiology, Independence Blue Cross Cardiovascular Research Center, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, U.S.A.
Correspondence: Dr Michael Autieri (email firstname.lastname@example.org).
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Clin Sci (Lond) (2016) 130 (22): 2101–2104.
August 10 2016
September 07 2016
September 09 2016
A commentary has been published: Adipose-specific inactivation of JNK alleviates atherosclerosis in apoE-deficient mice
Michael V. Autieri; Adipose inflammation at the heart of vascular disease. Clin Sci (Lond) 1 November 2016; 130 (22): 2101–2104. doi: https://doi.org/10.1042/CS20160628
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