期刊
NATURE CHEMICAL BIOLOGY
卷 8, 期 8, 页码 714-724出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/NCHEMBIO.1018
关键词
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资金
- Ministry of Education, Sciences, Sports and Technology, Japan
- Japan Science and Technology Agency PRESTO program
- Ministry of Health, Labor and Welfare of Japan
- US National Institutes of Health
- Grants-in-Aid for Scientific Research [22500337, 23651239, 24658122, 23659043, 23659166, 20117005, 20117001] Funding Source: KAKEN
An emerging aspect of redox signaling is the pathway mediated by electrophilic byproducts, such as nitrated cyclic nucleotide (for example, 8-nitroguanosine 3',5'-cyclic monophosphate (8-nitro-cGMP)) and nitro or keto derivatives of unsaturated fatty acids, generated via reactions of inflammation-related enzymes, reactive oxygen species, nitric oxide and secondary products. Here we report that enzymatically generated hydrogen sulfide anion (HS-) regulates the metabolism and signaling actions of various electrophiles. HS- reacts with electrophiles, best represented by 8-nitro-cGMP, via direct sulfhydration and modulates cellular redox signaling. The relevance of this reaction is reinforced by the significant 8-nitro-cGMP formation in mouse cardiac tissue after myocardial infarction that is modulated by alterations in HS- biosynthesis. Cardiac HS-, in turn, suppresses electrophile-mediated H-Ras activation and cardiac cell senescence, contributing to the beneficial effects of HS- on myocardial infarction-associated heart failure. Thus, this study reveals HS--induced electrophile sulfhydration as a unique mechanism for regulating electrophile-mediated redox signaling.
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