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Oxidative Medicine and Cellular Longevity
Volume 2016, Article ID 4529060, 8 pages
Review Article

Role of Endogenous Sulfur Dioxide in Regulating Vascular Structural Remodeling in Hypertension

1Department of Pediatrics, Peking University First Hospital, Beijing 100034, China
2University of California, San Diego, La Jolla, CA 92093, USA
3Department of Physiology and Pathophysiology, Peking University Health Science Center, Beijing 100191, China
4Key Lab of Molecular Cardiovascular Science of Ministry of Education, Beijing 100191, China

Received 22 March 2016; Accepted 21 July 2016

Academic Editor: Guangdong Yang

Copyright © 2016 Jia Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Sulfur dioxide (SO2), an emerging gasotransmitter, was discovered to be endogenously generated in the cardiovascular system. Recently, the physiological effects of endogenous SO2 were confirmed. Vascular structural remodeling (VSR), an important pathological change in many cardiovascular diseases, plays a crucial role in the pathogenesis of the diseases. Here, the authors reviewed the research progress of endogenous SO2 in regulating VSR by searching the relevant data from PubMed and Medline. In spontaneously hypertensive rats (SHRs) and pulmonary hypertensive rats, SO2/aspartate aminotransferase (AAT) pathway was significantly altered. SO2 inhibited vascular smooth muscle cell (VSMC) proliferation, promoted apoptosis, inhibited the synthesis of extracellular collagen but promoted its degradation, and enhanced antioxidative capacity, thereby playing a significant role in attenuating VSR. However, the detailed mechanisms needed to be further explored. Further studies in this field would be important for the better understanding of the pathogenesis of systemic hypertension and pulmonary hypertension. Also, clinical trials are needed to demonstrate if SO2 would be a potential therapeutic target in cardiovascular diseases.