It is believed that obesity has detrimental effects on the coronary circulation. These include immediate changes
in coronary arterial vasomotor responsiveness and the development of occlusive large coronary artery disease. Despite its
critical role in regulating myocardial perfusion, the altered behavior of coronary resistance arteries, which gives rise to
coronary microvascular disease (CMD) is poorly understood in obesity. A chronic, low-grade vascular inflammation has
been long considered as one of the main underlying pathology behind CMD. The expanded adipose tissue and the infiltrating
macrophages are the major sources of pro-inflammatory mediators that have been implicated in causing inadequate
myocardial perfusion and, in a long term, development of heart failure in obese patients. Much less is known the mechanisms
regulating the release of these cytokines into the circulation that enable them to exert their remote effects in the
coronary microcirculation. This mini review aims to examine recent studies describing alterations in the vasomotor function
of coronary resistance arteries and the role of adipose tissue-derived pro-inflammatory cytokines and adipokines in
contributing to CMD in obesity. We provide examples of regulatory mechanisms by which adipokines are released from
adipose tissue to exert their remote inflammatory effects on coronary microvessels. We identify some of the important
challenges and opportunities going forward.
Keywords: Obesity, coronary artery, adipose tissue, TNF, leptin, resistin, IL-6, adiponectin.
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