{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Shawky NM"],"funding":["NHLBI NIH HHS"],"pagination":["73-84"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4875816"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["32"],"pubmed_abstract":["Sulforaphane (SFN), a dietary phase-2 enzyme inducer that mitigates cellular oxidative stress through nuclear factor erythroid 2-related factor 2 (Nrf2) activation, is known to exhibit beneficial effects in the vessel wall. For instance, it inhibits vascular smooth muscle cell (VSMC) proliferation, a major event in atherosclerosis and restenosis after angioplasty. In particular, SFN attenuates the mitogenic and pro-inflammatory actions of platelet-derived growth factor (PDGF) and tumor necrosis factor-α (TNFα), respectively, in VSMCs. Nevertheless, the vasoprotective role of SFN has not been examined in the setting of obesity characterized by hyperleptinemia and insulin resistance. Using the mouse model of western diet-induced obesity, the present study demonstrates for the first time that"],"journal":["The Journal of nutritional biochemistry"],"pubmed_title":["Sulforaphane improves dysregulated metabolic profile and inhibits leptin-induced VSMC proliferation: Implications toward suppression of neointima formation after arterial injury in western diet-fed obese mice."],"pmcid":["PMC4875816"],"funding_grant_id":["R01 HL097090"],"pubmed_authors":["Pichavaram P","Suddek GM","Shawky NM","Jun JY","Segar L","Gameil NM","Shehatou GS"],"additional_accession":[]},"is_claimable":false,"name":"Sulforaphane improves dysregulated metabolic profile and inhibits leptin-induced VSMC proliferation: Implications toward suppression of neointima formation after arterial injury in western diet-fed obese mice.","description":"Sulforaphane (SFN), a dietary phase-2 enzyme inducer that mitigates cellular oxidative stress through nuclear factor erythroid 2-related factor 2 (Nrf2) activation, is known to exhibit beneficial effects in the vessel wall. For instance, it inhibits vascular smooth muscle cell (VSMC) proliferation, a major event in atherosclerosis and restenosis after angioplasty. In particular, SFN attenuates the mitogenic and pro-inflammatory actions of platelet-derived growth factor (PDGF) and tumor necrosis factor-α (TNFα), respectively, in VSMCs. Nevertheless, the vasoprotective role of SFN has not been examined in the setting of obesity characterized by hyperleptinemia and insulin resistance. Using the mouse model of western diet-induced obesity, the present study demonstrates for the first time that","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Jun","modification":"2025-04-19T15:03:42.631Z","creation":"2019-03-27T02:14:15Z"},"accession":"S-EPMC4875816","cross_references":{"pubmed":["27142739"],"doi":["10.1016/j.jnutbio.2016.01.009"]}}