Department of Nutrition, University of Petra, P.O. Box 961343, Amman 11196, Jordan.
Department of Pharmacology and Therapeutics, Beirut Arab University, P.O. Box 11-5020, Beirut 1107-2809, Lebanon.
Int J Mol Sci. 2020 Nov 20;21(22):8764. doi: 10.3390/ijms21228764.
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.
活性氧（ROS）是细胞内氧代谢的天然副产物。在生理水平下，它们在细胞信号转导中起着至关重要的作用。然而，高水平的 ROS 会导致氧化应激，这与心血管疾病（CVD）如动脉粥样硬化、高血压和血管成形术后再狭窄有关。尽管已经进行了大量研究来确定 ROS 在 CVD 中的作用，但图像仍然远不完整。CVD 病理生理学中的一个常见事件是血管平滑肌细胞（VSMCs）从收缩型向合成型表型的转变。有趣的是，氧化应激是这种表型转变的主要原因。在这篇综述中，我们重点关注 ROS 对 VSMC 表型转变特征的影响，特别是增殖和迁移。此外，我们还推测了这些细胞事件的潜在分子机制。沿着这些思路，我们深入讨论了 ROS 对 VSMCs 收缩标志物表达的影响。最后，我们评论了抗氧化剂作为 CVD 治疗的效率。
