Journal
FASEB JOURNAL
Volume 33, Issue 12, Pages 13098-13125Publisher
WILEY
DOI: 10.1096/fj.201901304R
Keywords
H2S; metabolism; ROS; apoptosis; persulfidation
Categories
Funding
- U.S. National Institutes of Health (NIH) National Cancer Institute (NCI) [2R01CA136494, CA213278]
- NIH National Heart, Lung, and Blood Institute [HL120585]
- NCI Cancer Center Support Grant [P30CA225520]
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Hydrogen sulfide can signal through 3 distinct mechanisms: 1) reduction and/or direct binding of metalloprotein heme centers, 2) serving as a potent antioxidant through reactive oxygen species/reactive nitrogen species scavenging, or 3) post-translational modification of proteins by addition of a thiol (-SH) group onto reactive cysteine residues: a process known as persulfidation. Below toxic levels, hydrogen sulfide promotes mitochondrial biogenesis and function, thereby conferring protection against cellular stress. For these reasons, increases in hydrogen sulfide and hydrogen sulfide-producing enzymes have been implicated in several human disease states. This review will first summarize our current understanding of hydrogen sulfide production and metabolism, as well as its signaling mechanisms; second, this work will detail the known mechanisms of hydrogen sulfide in the mitochondria and the implications of its mitochondrial-specific impacts in several pathologic conditions.
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