ArticleAntioxidants & redox signaling2014
Sulfhydration of p66Shc at cysteine59 mediates the antioxidant effect of hydrogen sulfide.
Article in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 128 citations in OpenAlex.
- S-sulfhydration: Novel insights into the antioxidant and antiinflammation in age-related diseases.Journal of advanced research · 2026Review
- Epigenetic and O-glycosylation regulation of p66Shc mitigates mitochondrial oxidative stress in aortic dissection.Theranostics · 2026Article
- Hydrogen sulfide protects against spinal cord pyroptosis via persulfidation of Rac1 after lumbosacral plexus nerve injury.Cell death discovery · 2025Article
- Hydrogen Sulfide Protects Erectile Function Through Stimulation of Antioxidant Defense in the Corpus Cavernosum: Insights From SG1002 Administration and Cystathionine γ-Lyase Knockout.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- p66Shc deletion confers apoptotic resistance to loss of EGFR-ERK signalling in neural stem cells.Cell death & disease · 2025Article
- GYY4137-induced p65 sulfhydration protects synovial macrophages against pyroptosis by improving mitochondrial function in osteoarthritis development.Journal of advanced research · 2025Article
- Gut Microbiota and Their Metabolites: The Hidden Driver of Diabetic Nephropathy? Unveiling Gut Microbe's Role in DN.Journal of diabetes · 2025Review
- Neurogasobiology of migraine: Carbon monoxide, hydrogen sulfide, and nitric oxide as emerging pathophysiological trinacrium relevant to nociception regulation.Open medicine (Warsaw, Poland) · 2025Review
- The interplay of hydrogen sulfide and microRNAs in cardiovascular diseases: insights and future perspectives.Mammalian genome : official journal of the International Mammalian Genome Society · 2024Review
- Review
- Review
- Targeted HBiomaterials research · 2024Article
- Reduced hydrogen sulfide production contributes to adrenal insufficiency induced by hypoxia via modulation of NLRP3 inflammasome activation.Redox report : communications in free radical research · 2023Article
- The roles of hydrogen sulfide in renal physiology and disease states.Renal failure · 2022Review
- Recent Development of the Molecular and Cellular Mechanisms of Hydrogen Sulfide Gasotransmitter.Antioxidants (Basel, Switzerland) · 2022Review
- Homocysteinylation and Sulfhydration in Diseases.Current neuropharmacology · 2022Review
- Emerging roles of cystathionine β-synthase in various forms of cancer.Redox biology · 2022Review
- p66Shc in Cardiovascular Pathology.Cells · 2022Review
- The Interplay between Hydrogen Sulfide and Phytohormone Signaling Pathways under Challenging Environments.International journal of molecular sciences · 2022Review
- Sp1 S-Sulfhydration Induced by Hydrogen Sulfide Inhibits Inflammation via HDAC6/MyD88/NF-κB Signaling Pathway in Adjuvant-Induced Arthritis.Antioxidants (Basel, Switzerland) · 2022Article
3 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsMitochondrion is considered as the major source of intracellular reactive oxygen species (ROS). H2S has been reported to be an antioxidant, but its mechanism remains largely elusive. P66Shc is an upstream activator of mitochondrial redox signaling. The aim of this study was to explore whether the antioxidant effect of H2S is mediated by p66Shc.
resultsApplication of exogenous H2S with its donor, NaHS, or overexpression of its generating enzyme, cystathionine β-synthase, induced sulfhydration of p66Shc, but inhibited its phosphorylation caused by H2O2/D-galactose in SH-SY5Y cells or in the mice cortex. H2S also decreased mitochondrial ROS production and protected neuronal cells against stress-induced senescence. PKCβII and PP2A are the two key proteins to regulate p66Shc phosphorylation. Although H2S failed to affect the activities of these two proteins, it disrupted their association. Cysteine-59 resides in proximity to serine-36, the phosphorylation site of p66Shc. The C59S mutant attenuated the above-described biological function of H2S. INNOVATION: We revealed a novel mechanism for the antioxidant effect of H2S and its role in oxidative stress-related diseases.
conclusionH2S inhibits mitochondrial ROS production via the sulfhydration of Cys-59 residue, which in turn, prevents the phosphorylation of p66Shc.
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