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Oxidative Medicine and Cellular Longevity
Volume 2015, Article ID 758678, 9 pages
Review Article

Interaction of Hydrogen Sulfide with Oxygen Sensing under Hypoxia

1Department of Pathophysiology, Harbin Medical University, Harbin 150086, China
2Joint Research Center for Bone and Joint Disease, Model Animal Research Center, Nanjing University, Nanjing 210093, China
3Department of Geriatrics, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China

Received 30 November 2014; Accepted 22 January 2015

Academic Editor: Steven S. An

Copyright © 2015 Bo Wu 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.


Based on the discovery of endogenous H2S production, many in depth studies show this gasotransmitter with a variety of physiological and pathological functions. Three enzymes, cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (MST), are involved in enzymatic production of H2S. Emerging evidence has elucidated an important protective role of H2S in hypoxic conditions in many mammalian systems. However, the mechanisms by which H2S senses and responses to hypoxia are largely elusive. Hypoxia-inducible factors (HIFs) function as key regulators of oxygen sensing, activating target genes expression under hypoxia. Recent studies have shown that exogenous H2S regulates HIF action in different patterns. The activation of carotid bodies is a sensitive and prompt response to hypoxia, rapidly enhancing general O2 supply. H2S has been identified as an excitatory mediator of hypoxic sensing in the carotid bodies. This paper presents a brief review of the roles of these two pathways which contribute to hypoxic sensing of H2S.