Key result
Visceral fat JNK inactivation curbs systemic inflammation and reduces atherosclerosis development.
Why the study?
Visceral adipose tissue is a primary site of chronic inflammation in obesity and may contribute to systemic inflammation and development of atherosclerotic vascular disease, but molecular mechanisms and secretory pathways mediating this process are not well identified.
Hypothesis-generating for adipose JNK targeting in atherosclerosis; leaves open human translation pending clinical studies.
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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Michael V. Autieri (2016) conducted an editorial in Atherosclerotic vascular disease. Adipose-specific inactivation of JNK (dnJNK expression) vs. Control mice was evaluated on Atherosclerotic lesion formation and systemic inflammation. Selective inactivation of JNK in visceral adipose tissue reduced systemic inflammation and significantly decreased the development of atherosclerosis in ApoE-/- mice.
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