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Sulfur dioxide acts as a novel endogenous gaseous signaling molecule in the cardiovascular system.

AbstractOBJECTIVE:
Sulfur dioxide was considered to be toxic and detrimental to human health. However, this review highlights recent advances that suggest sulfur dioxide might be a novel endogenous gaseous signaling molecule involved in the regulation of cardiovascular functions.
DATA SOURCES:
The data used in this review were mainly from the studies reported in Medline and PubMed published from 1986 to 2010.
STUDY SELECTION:
Original articles and critical reviews selected were relevant to exogenous and endogenous sulfur dioxide.
RESULTS:
The sulfur dioxide/aspartate amino transferase pathway is endogenously generated in the cardiovascular system, and sulfur dioxide shows broad bioactive effects, such as antihypertension, vasodilation, and amelioration of vascular remodeling. A disturbed sulfur dioxide/aspartate amino transferase pathway is known to be involved in the pathogenesis of many cardiovascular diseases, such as ischemia-reperfusion injury, monocrotaline-induced pulmonary hypertension, athrosclerosis, spontaneous hypertension and hypoxic pulmonary hypertension. Furthermore, in experimental studies the prognosis of these cardiovascular diseases can be improved by targeting endogenous sulfur dioxide.
CONCLUSION:
The findings suggest that sulfur dioxide is a novel endogenous gaseous signaling molecule involved in the regulation of cardiovascular functions.
AuthorsShan-Shan Chen, Chao-Shu Tang, Hong-Fang Jin, Jun-Bao DU
JournalChinese medical journal (Chin Med J (Engl)) Vol. 124 Issue 12 Pg. 1901-5 (Jun 2011) ISSN: 2542-5641 [Electronic] China
PMID21740851 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Chemical References
  • Sulfur Dioxide
Topics
  • Animals
  • Cardiovascular Diseases (etiology)
  • Humans
  • Hypertension, Pulmonary (etiology)
  • Myocardial Reperfusion Injury (etiology)
  • Rats
  • Rats, Inbred SHR
  • Signal Transduction (physiology)
  • Sulfur Dioxide (metabolism)

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