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Protein S‐sulfhydration by hydrogen sulfide in cardiovascular system
Author(s) -
Meng Guoliang,
Zhao Shuang,
Xie Liping,
Han Yi,
Ji Yong
Publication year - 2018
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/bph.13825
Subject(s) - cysteine , chemistry , biochemistry , cysteine metabolism , protein tyrosine phosphatase , phosphatase , enzyme
Hydrogen sulfide (H 2 S), independently of any specific transporters, has a number of biological effects on the cardiovascular system. However, until now, the detailed mechanism of H 2 S was not clear. Recently, a novel post-translational modification induced by H 2 S, named S-sulfhydration, has been proposed. S-sulfhydration is the chemical modification of specific cysteine residues of target proteins by H 2 S. There are several methods for detecting S-sulfhydration, such as the modified biotin switch assay, maleimide assay with fluorescent thiol modifying regents, tag-switch method and mass spectrometry. H 2 S induces S-sulfhydration on enzymes or receptors (such as p66Shc, phospholamban, protein tyrosine phosphatase 1B, mitogen-activated extracellular signal-regulated kinase 1 and ATP synthase subunit α), transcription factors (such as specific protein-1, kelch-like ECH-associating protein 1, NF-κB and interferon regulatory factor-1), and ion channels (such as voltage-activated Ca 2+ channels, transient receptor potential channels and ATP-sensitive K + channels) in the cardiovascular system. Although significant progress has been achieved in delineating the role of protein S-sulfhydration by H 2 S in the cardiovascular system, more proteins with detailed cysteine sites of S-sulfhydration as well as physiological function need to be investigated in further studies. This review mainly summarizes the role and possible mechanism of S-sulfhydration in the cardiovascular system. The S-sulfhydrated proteins may be potential novel targets for therapeutic intervention and drug design in the cardiovascular system, which may accelerate the development and application of H 2 S-related drugs in the future.