scholarly journals MiR-26a contributes to the PDGF-BB-induced phenotypic switch of vascular smooth muscle cells by suppressing Smad1

Oncotarget ◽  
2017 ◽  
Vol 8 (44) ◽  
pp. 75844-75853 ◽  
Author(s):  
Xiaoyan Yang ◽  
Mei Dong ◽  
Hao Wen ◽  
Xiaoling Liu ◽  
Meng Zhang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Phenotypic Switch

The epigenetic phenotypic switch of vascular smooth muscle cells involved in atherosclerosis

The Lancet ◽  
2013 ◽  
Vol 381 ◽  
pp. S34 ◽  
Author(s):  
Mark Davies ◽  
Jennifer Harman ◽  
Haixiang Yu ◽  
Martin Bennett ◽  
Helle Jørgensen
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Phenotypic Switch

scholarly journals Reactive Oxygen Species: Modulators of Phenotypic Switch of Vascular Smooth Muscle Cells

2020 ◽  
Vol 21 (22) ◽  
pp. 8764
Author(s):  
Adnan Badran ◽  
Suzanne A. Nasser ◽  
Joelle Mesmar ◽  
Ahmed F. El-Yazbi ◽  
Alessandra Bitto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Reactive Oxygen ◽  
Muscle Cells ◽  
Oxygen Species ◽  
Phenotypic Switch

Reactive oxygen species (ROS) are natural byproducts of oxygen metabolism in the cell. At physiological levels, they play a vital role in cell signaling. However, high ROS levels cause oxidative stress, which is implicated in cardiovascular diseases (CVD) such as atherosclerosis, hypertension, and restenosis after angioplasty. Despite the great amount of research conducted to identify the role of ROS in CVD, the image is still far from being complete. A common event in CVD pathophysiology is the switch of vascular smooth muscle cells (VSMCs) from a contractile to a synthetic phenotype. Interestingly, oxidative stress is a major contributor to this phenotypic switch. In this review, we focus on the effect of ROS on the hallmarks of VSMC phenotypic switch, particularly proliferation and migration. In addition, we speculate on the underlying molecular mechanisms of these cellular events. Along these lines, the impact of ROS on the expression of contractile markers of VSMCs is discussed in depth. We conclude by commenting on the efficiency of antioxidants as CVD therapies.

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