dc.creatorReichert
dc.creatorKarla; Pereira do Carmo
dc.creatorHelison Rafael; Torina
dc.creatorAnali Galluce; de Carvalho
dc.creatorDaniela Diogenes; Sposito
dc.creatorAndrei Carvalho; de Souza Vilarinho
dc.creatorKarlos Alexandre; Silveira-Filho
dc.creatorLindemberg da Mota; Martins de Oliveira
dc.creatorPedro Paulo; Petrucci
dc.creatorOrlando
dc.date2016
dc.datenov
dc.date2017-11-13T13:45:42Z
dc.date2017-11-13T13:45:42Z
dc.date.accessioned2018-03-29T06:00:23Z
dc.date.available2018-03-29T06:00:23Z
dc.identifierPlos One. Public Library Science, v. 11, p. , 2016.
dc.identifier1932-6203
dc.identifierWOS:000388889500038
dc.identifier10.1371/journal.pone.0166845
dc.identifierhttp://journals.plos.org/plosone/article?id=10.1371/journal.pone.0166845
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/329077
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1366102
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionTherapeutic strategies that modulate ventricular remodeling can be useful after acute myocardial infarction (MI). In particular, statins may exert effects on molecular pathways involved in collagen metabolism. The aim of this study was to determine whether treatment with atorvastatin for 4 weeks would lead to changes in collagen metabolism and ventricular remodeling in a rat model of MI. Methods Male Wistar rats were used in this study. MI was induced in rats by ligation of the left anterior descending coronary artery (LAD). Animals were randomized into three groups, according to treatment: sham surgery without LAD ligation (sham group, n = 14), LAD ligation followed by 10mg atorvastatin/kg/day for 4 weeks (atorvastatin group, n = 24), or LAD ligation followed by saline solution for 4 weeks (control group, n = 27). After 4 weeks, hemodynamic characteristics were obtained by a pressure-volume catheter. Hearts were removed, and the left ventricles were subjected to histologic analysis of the extents of fibrosis and collagen deposition, as well as the myocyte cross-sectional area. Expression levels of mediators involved in collagen metabolism and inflammation were also assessed. Results End-diastolic volume, fibrotic content, and myocyte cross-sectional area were significantly reduced in the atorvastatin compared to the control group. Atorvastatin modulated expression levels of proteins related to collagen metabolism, including MMP1, TIMP1, COL I, PCPE, and SPARC, in remote infarct regions. Atorvastatin had anti-inflammatory effects, as indicated by lower expression levels of TLR4, IL-1, and NF-kB p50. Conclusion Treatment with atorvastatin for 4 weeks was able to attenuate ventricular dysfunction, fibrosis, and left ventricular hypertrophy after MI in rats, perhaps in part through effects on collagen metabolism and inflammation. Atorvastatin may be useful for limiting ventricular remodeling after myocardial ischemic events.
dc.description11
dc.description11
dc.descriptionFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [2013/10661-4, 2012/09494-3, 2012/09130-1, 2011/14550-7]
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.languageEnglish
dc.publisherPublic Library Science
dc.publisherSan Francisco
dc.relationPlos One
dc.rightsaberto
dc.sourceWOS
dc.titleAtorvastatin Improves Ventricular Remodeling After Myocardial Infarction By Interfering With Collagen Metabolism
dc.typeArtículos de revistas


Este ítem pertenece a la siguiente institución