{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["58"],"submitter":["Yin YL"],"funding":["National Natural Science Foundation of China"],"pubmed_abstract":["<h4>Background</h4>s: Hyperhomocysteinemia (HHcy) is one of risk factors for vascular cognitive impairment (VCI). GTP cyclohydrolase 1 (GCH1) deficiency is critical to oxidative stress in vascular dysfunction. The aim of this study was designed to examine whether HHcy induces VCI through GCH1 S-nitrosylation, a redox-related post-translational modification of cysteine.<h4>Methods</h4>The VCI model was induced by feeding mice homocysteine thiolactone (HTL) for 16 consecutive weeks. The cognitive functions were evaluated by step-down avoidance test, passive avoidance step-through task test, and Morris water maze (MWM) test. Protein S-nitrosylation was assayed using a biotin-switch method.<h4>Results</h4>In cell-free system, nitric oxide (NO) donor induced GCH1 protein S-nitrosylation and dec"],"journal":["Redox biology"],"pagination":["102540"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9673109"],"repository":["biostudies-literature"],"pubmed_title":["Nitrosative stress induced by homocysteine thiolactone drives vascular cognitive impairments via GTP cyclohydrolase 1 S-nitrosylation in vivo."],"pmcid":["PMC9673109"],"pubmed_authors":["Lu JX","Wang SX","Li P","Bai YP","Yin YL","Wang JZ","Wang L","Ren F","Lu CB","Chen Y","Zhu ML","Liu C","Wang QQ"],"additional_accession":[]},"is_claimable":false,"name":"Nitrosative stress induced by homocysteine thiolactone drives vascular cognitive impairments via GTP cyclohydrolase 1 S-nitrosylation in vivo.","description":"<h4>Background</h4>s: Hyperhomocysteinemia (HHcy) is one of risk factors for vascular cognitive impairment (VCI). GTP cyclohydrolase 1 (GCH1) deficiency is critical to oxidative stress in vascular dysfunction. The aim of this study was designed to examine whether HHcy induces VCI through GCH1 S-nitrosylation, a redox-related post-translational modification of cysteine.<h4>Methods</h4>The VCI model was induced by feeding mice homocysteine thiolactone (HTL) for 16 consecutive weeks. The cognitive functions were evaluated by step-down avoidance test, passive avoidance step-through task test, and Morris water maze (MWM) test. Protein S-nitrosylation was assayed using a biotin-switch method.<h4>Results</h4>In cell-free system, nitric oxide (NO) donor induced GCH1 protein S-nitrosylation and dec","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Nov","modification":"2025-04-18T14:59:31.812Z","creation":"2025-04-07T01:24:12.654Z"},"accession":"S-EPMC9673109","cross_references":{"pubmed":["36399957"],"doi":["10.1016/j.redox.2022.102540"]}}