{'fraction_non_alphanumeric': 0.03372681281618887, 'fraction_numerical': 0.008431703204047217, 'mean_word_length': 6.26530612244898, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Protein S‐sulfhydration by hydrogen sulfide in cardiovascular system

Hydrogen sulfide (H2S), independently of any specific transporters, has a number of biological effects on the cardiovascular system. However, until now, the detailed mechanism of H2S was not clear. Recently, a novel post‐translational modification induced by H2S, named S‐sulfhydration, has been proposed. S‐sulfhydration is the chemical modification of specific cysteine residues of target proteins by H2S. 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. H2S 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 Ca2+ 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 H2S 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 H2S‐related drugs in the future.