Key result
Excess matrix metalloproteinase production from macrophages, driven by multiple inflammatory mediators, contributes to extracellular matrix destruction and atherosclerotic plaque rupture.
Design
Review
Authors
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Warrants human-specific MMP studies in atherosclerosis; leaves open clinical translation from macrophage mechanisms.
Understanding the divergent regulation of MMPs and TIMPs between human and mouse macrophages provides insights into the mechanisms of atherosclerotic plaque rupture and potential therapeutic targets.
Andrew C. Newby (2016) conducted a review in Atherosclerosis and myocardial infarction. Matrix metalloproteinase (MMP) production from macrophages was evaluated. Excess matrix metalloproteinase production from macrophages, driven by multiple inflammatory mediators, contributes to extracellular matrix destruction and atherosclerotic plaque rupture.
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