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Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
Published on: September 26, 2018
Adiponectin and vulnerable atherosclerotic plaques.
Ailin Barseghian1, Dipika Gawande, Mandeep Bajaj
1University of California, Irvine, California, USA.
Journal of the American College of Cardiology
|February 12, 2011
Summary
Vulnerable plaque rupture in coronary artery disease is linked to specific features and low adiponectin levels. Adiponectin may play a role in the inflammatory processes driving atherosclerosis progression.
Area of Science:
- Cardiovascular Medicine
- Endocrinology
- Pathology
Background:
- High-risk plaques prone to rupture exhibit distinct morphology: large necrotic cores, thin fibrous caps, and positive remodeling.
- Stable coronary artery disease lesions differ morphologically from rupture-prone plaques.
- Adiponectin, an adipocytokine, is decreased in obesity and type 2 diabetes.
Purpose of the Study:
- To explore the role of adiponectin in coronary artery disease progression.
- To investigate the association between hypoadiponectinemia and increased risk of coronary artery disease and acute coronary syndrome.
Main Methods:
- Morphological analysis of coronary plaques.
- Assessment of adiponectin levels in patients with coronary artery disease.
- Correlation analysis between adiponectin levels, plaque characteristics, and clinical outcomes.
Main Results:
- Distinct morphological features characterize high-risk, rupture-vulnerable plaques.
- Hypoadiponectinemia is associated with an increased risk of coronary artery disease and acute coronary syndrome in some studies.
- Adiponectin levels correlate with inflammatory and atherogenic mechanisms in pathological coronary disease.
Conclusions:
- Adiponectin levels offer insights into the inflammatory and atherogenic pathways of coronary atherosclerosis.
- Understanding adiponectin's role may elucidate mechanisms underlying vulnerable plaque formation and rupture.
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