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Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation
Published on: April 3, 2017
Obesity and coronary microvascular disease - implications for adipose tissue-mediated remote inflammatory response
Zsolt Bagi, Zuzana Broskova, Attila Feher1
1Vascular Biology Center, Medical College of Georgia, Georgia Regents University, Augusta, GA, USA. zbagi@gru.edu.
Insights
Obesity impairs coronary circulation, leading to coronary microvascular disease (CMD) via chronic inflammation. Adipose tissue releases inflammatory mediators affecting coronary arteries, contributing to heart failure in obese individuals.
Area of Science:
- Cardiovascular Physiology
- Obesity Pathophysiology
- Vascular Inflammation
Background:
- Obesity negatively impacts coronary circulation, causing vasomotor dysfunction and coronary artery disease.
- Coronary microvascular disease (CMD) in obesity is poorly understood, though chronic inflammation is a key factor.
- Adipose tissue and macrophages release pro-inflammatory mediators contributing to inadequate myocardial perfusion and heart failure.
Purpose of the Study:
- To review recent studies on coronary resistance artery vasomotor function in obesity.
- To examine the role of adipose tissue-derived cytokines and adipokines in obesity-related CMD.
- To explore mechanisms of adipokine release and their remote inflammatory effects on coronary microvessels.
Main Methods:
- Literature review of recent studies on obesity and coronary microcirculation.
- Analysis of mechanisms linking adipose tissue inflammation to coronary microvascular dysfunction.
- Examination of adipokine signaling pathways in the context of obesity and cardiovascular health.
Main Results:
- Obesity alters coronary resistance artery vasomotor function.
- Adipose tissue-derived pro-inflammatory cytokines and adipokines are key contributors to CMD.
- Specific regulatory mechanisms for adipokine release and their impact on coronary microvessels are elucidated.
Conclusions:
- Obesity-induced chronic inflammation and altered adipokine signaling significantly contribute to coronary microvascular disease.
- Understanding these mechanisms is crucial for developing therapeutic strategies to prevent heart failure in obese patients.
- Further research is needed to fully elucidate the complex interplay between adipose tissue, inflammation, and coronary microvascular function.
Abstract:
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.
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