Cholesterol-Induced Phenotypic Modulation of Smooth Muscle Cells to Macrophage/Fibroblast-like Cells Is Driven by an Unfolded Protein Response.

CONCLUSIONS: Our data demonstrate that UPR is necessary and sufficient to drive phenotypic switching of SMCs to cells that resemble modulated SMCs found in atherosclerotic plaques. Preventing a UPR in hyperlipidemic mice diminishes atherosclerotic burden, and our data suggest that preventing SMC transition to dedifferentiated cells expressing macrophage and fibroblast markers contributes to this decreased plaque burden.
PMID: 33028096 [PubMed - as supplied by publisher]

Source: Arteriosclerosis, Thrombosis and Vascular Biology - October 8, 2020 Category: Cardiology Authors: Chattopadhyay A, Kwartler CS, Kaw K, Li Y, Kaw A, Chen J, LeMaire SA, Shen YH, Milewicz DM Tags: Arterioscler Thromb Vasc Biol Source Type: research