Key result
OxLDL-activated monocytes promote vascular smooth muscle cell phenotypic switch through NLRP3 inflammasome activation, likely contributing to atherosclerotic plaque instability.
Why the study?
It remained to be investigated whether monocytes and NLRP3 inflammasome activation are direct triggers of vascular smooth muscle cell phenotypic switch and plaque disruption.
Does monocyte-induced NLRP3 inflammasome activation promote vascular smooth muscle cell phenotypic switch in atherosclerosis?
Population
VSMC co-cultures, VSMC lineage tracing mice, and human carotid atherosclerotic plaques
Comparison
OxLDL-activated monocytes vs controls in vitro, and high cholesterol vs normal diet in mice
Design
In vitro co-culture and in vivo preclinical and human translational study
Authors
Loading...
Monocyte NLRP3 activation may promote VSMC phenotypic switch in plaques; leaves open targeted inhibition for stability.
Does monocyte-induced NLRP3 inflammasome activation promote vascular smooth muscle cell phenotypic switch in atherosclerosis?
Monocyte-induced NLRP3 inflammasome activation drives vascular smooth muscle cell phenotypic switching, highlighting a mechanism for atherosclerotic plaque destabilization.
Burger et al. (2021) studied Atherosclerosis. OxLDL-activated monocytes and NLRP3 inflammasome activation was evaluated on VSMC phenotypic switch and NLRP3 inflammasome activation. OxLDL-activated monocytes promote vascular smooth muscle cell phenotypic switch through NLRP3 inflammasome activation, likely contributing to atherosclerotic plaque instability.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: