Reactive Oxygen Species: Modulators of Phenotypic Switch of Vascular Smooth Muscle Cells
Open Access
- 20 November 2020
- journal article
- review article
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 21 (22), 8764
- https://doi.org/10.3390/ijms21228764
Abstract
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.This publication has 159 references indexed in Scilit:
- Mechanisms of oxidative stress in human aortic aneurysms — Association with clinical risk factors for atherosclerosis and disease severityInternational Journal of Cardiology, 2013
- Regulation of reactive oxygen species by p53: implications for nitric oxide-mediated apoptosisAmerican Journal of Physiology-Heart and Circulatory Physiology, 2010
- Oxidative Stress and Vascular Smooth Muscle Cell Growth: A Mechanistic Linkage by Cyclophilin AAntioxidants and Redox Signaling, 2010
- Redox Control of Vascular Smooth Muscle MigrationAntioxidants and Redox Signaling, 2010
- Peroxide generation by p47phox-Src activation of Nox2 has a key role in protein kinase C-induced arterial smooth muscle contractionAmerican Journal of Physiology-Heart and Circulatory Physiology, 2009
- Superoxide dismutase 1 (SOD1) is essential for H 2 O 2 -mediated oxidation and inactivation of phosphatases in growth factor signalingProceedings of the National Academy of Sciences of the United States of America, 2008
- Oxidative Stress Induces Vascular Calcification through Modulation of the Osteogenic Transcription Factor Runx2 by AKT SignalingJournal of Biological Chemistry, 2008
- Myocardin inhibits cellular proliferation by inhibiting NF-κB(p65)-dependent cell cycle progressionProceedings of the National Academy of Sciences of the United States of America, 2008
- Reactive oxygen species signaling in vascular smooth muscle cellsCardiovascular Research, 2006
- The pathogenesis of atherosclerosis: a perspective for the 1990sNature, 1993