<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Shawky NM</submitter><funding>NHLBI NIH HHS</funding><pagination>73-84</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4875816</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>32</volume><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</pubmed_abstract><journal>The Journal of nutritional biochemistry</journal><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.</pubmed_title><pmcid>PMC4875816</pmcid><funding_grant_id>R01 HL097090</funding_grant_id><pubmed_authors>Pichavaram P</pubmed_authors><pubmed_authors>Suddek GM</pubmed_authors><pubmed_authors>Shawky NM</pubmed_authors><pubmed_authors>Jun JY</pubmed_authors><pubmed_authors>Segar L</pubmed_authors><pubmed_authors>Gameil NM</pubmed_authors><pubmed_authors>Shehatou GS</pubmed_authors></additional><is_claimable>false</is_claimable><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.</name><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</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Jun</publication><modification>2025-04-19T15:03:42.631Z</modification><creation>2019-03-27T02:14:15Z</creation></dates><accession>S-EPMC4875816</accession><cross_references><pubmed>27142739</pubmed><doi>10.1016/j.jnutbio.2016.01.009</doi></cross_references></HashMap>