scholarly journals Precise theranostic nanomedicines for inhibiting vulnerable atherosclerotic plaque progression through regulation of vascular smooth muscle cell phenotype switching

Theranostics ◽  
2018 ◽  
Vol 8 (13) ◽  
pp. 3693-3706 ◽  
Author(s):  
Sai Ma ◽  
Seyed Mohammad Motevalli ◽  
Jiangwei Chen ◽  
Meng-Qi Xu ◽  
Yabin Wang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Atherosclerotic Plaque ◽  
Cell Phenotype ◽  
Plaque Progression ◽  
Vulnerable Atherosclerotic Plaque ◽  
Smooth Muscle Cell Phenotype ◽  
Phenotype Switching

scholarly journals Vascular smooth muscle cell phenotype switching in carotid atherosclerosis

2021 ◽  
Author(s):  
Elizabeth L. Chou ◽  
Christian L. Lino Cardenas ◽  
Mark Chaffin ◽  
Alessandro Arduini ◽  
Dejan Juric ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Carotid Atherosclerosis ◽  
Cell Phenotype ◽  
Smooth Muscle Cell Phenotype ◽  
Phenotype Switching

scholarly journals Epigenetic Regulation of Vascular Smooth Muscle Cell Phenotype Switching in Atherosclerotic Artery Remodeling: A Mini-Review

2021 ◽  
Vol 12 ◽  
Author(s):  
Michelle Zurek ◽  
Einari Aavik ◽  
Rahul Mallick ◽  
Seppo Ylä-Herttuala
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Cell Phenotype ◽  
Arterial Remodeling ◽  
Vascular Walls ◽  
Smooth Muscle Cell Phenotype ◽  
Phenotype Switching

Atherosclerosis is a chronic inflammatory disease characterized by extensive remodeling of medium and large-sized arteries. Inward remodeling (=lumen shrinkage) of the vascular walls is the underlying cause for ischemia in target organs. Therefore, inward remodeling can be considered the predominant feature of atherosclerotic pathology. Outward remodeling (=lumen enlargement) is a physiological response compensating for lumen shrinkage caused by neointimal hyperplasia, but as a pathological response to changes in blood flow, outward remodeling leads to substantial arterial wall thinning. Thinned vascular walls are prone to rupture, and subsequent thrombus formation accounts for the majority of acute cardiovascular events. Pathological remodeling is driven by inflammatory cells which induce vascular smooth muscle cells to switch from quiescent to a proliferative and migratory phenotype. After decades of intensive research, the molecular mechanisms of arterial remodeling are starting to unfold. In this mini-review, we summarize the current knowledge of the epigenetic and transcriptional regulation of vascular smooth muscle cell phenotype switching from the contractile to the synthetic phenotype involved in arterial remodeling and discuss potential therapeutic options.

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