دورية أكاديمية

Atorvastatin Improves Ventricular Remodeling after Myocardial Infarction by Interfering with Collagen Metabolism.

التفاصيل البيبلوغرافية
العنوان: Atorvastatin Improves Ventricular Remodeling after Myocardial Infarction by Interfering with Collagen Metabolism.
المؤلفون: Reichert K; Laboratory of Myocardial Ischemia/Reperfusion, Faculty of Medical Science, State University of Campinas - UNICAMP, Campinas, SP, Brazil., Pereira do Carmo HR; Laboratory of Myocardial Ischemia/Reperfusion, Faculty of Medical Science, State University of Campinas - UNICAMP, Campinas, SP, Brazil., Galluce Torina A; Laboratory of Myocardial Ischemia/Reperfusion, Faculty of Medical Science, State University of Campinas - UNICAMP, Campinas, SP, Brazil., Diógenes de Carvalho D; Laboratory of Myocardial Ischemia/Reperfusion, Faculty of Medical Science, State University of Campinas - UNICAMP, Campinas, SP, Brazil., Carvalho Sposito A; Department of Internal Medicine, Faculty of Medical Science, State University of Campinas - UNICAMP, Campinas, SP, Brazil., de Souza Vilarinho KA; Department of Surgery, Discipline of Cardiac Surgery, Faculty of Medical Science, State University of Campinas - UNICAMP, Campinas, SP, Brazil., da Mota Silveira-Filho L; Department of Surgery, Discipline of Cardiac Surgery, Faculty of Medical Science, State University of Campinas - UNICAMP, Campinas, SP, Brazil., Martins de Oliveira PP; Department of Surgery, Discipline of Cardiac Surgery, Faculty of Medical Science, State University of Campinas - UNICAMP, Campinas, SP, Brazil., Petrucci O; Laboratory of Myocardial Ischemia/Reperfusion, Faculty of Medical Science, State University of Campinas - UNICAMP, Campinas, SP, Brazil.; Department of Surgery, Discipline of Cardiac Surgery, Faculty of Medical Science, State University of Campinas - UNICAMP, Campinas, SP, Brazil.; Section of Pediatric Cardiothoracic Surgery, Department of Surgery, Washington University School of Medicine, St. Louis, Missouri, United States of America.
المصدر: PloS one [PLoS One] 2016 Nov 23; Vol. 11 (11), pp. e0166845. Date of Electronic Publication: 2016 Nov 23 (Print Publication: 2016).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science
مواضيع طبية MeSH: Anticholesteremic Agents/*pharmacology , Atorvastatin/*pharmacology , Collagen/*metabolism , Ventricular Remodeling/*drug effects, Animals ; Anticholesteremic Agents/therapeutic use ; Atorvastatin/therapeutic use ; Catheter Ablation ; Disease Models, Animal ; Fibrosis ; Gene Expression/drug effects ; Heart Ventricles/pathology ; Hemodynamics/drug effects ; Interleukin-1/genetics ; Interleukin-1/metabolism ; Male ; Matrix Metalloproteinase 1/metabolism ; Myocardial Infarction/drug therapy ; Myocardial Infarction/pathology ; Myocardial Infarction/surgery ; Myocardium/metabolism ; Myocardium/pathology ; NF-kappa B p50 Subunit/genetics ; NF-kappa B p50 Subunit/metabolism ; Rats ; Rats, Wistar ; Tissue Inhibitor of Metalloproteinase-1/metabolism
مستخلص: Purpose: Therapeutic 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.
Competing Interests: The authors have declared that no competing interests exist.
التعليقات: Erratum in: PLoS One. 2017 Feb 14;12 (2):e0172453. (PMID: 28196119)
References: Arch Immunol Ther Exp (Warsz). 2009 May-Jun;57(3):165-76. (PMID: 19479203)
J Hypertens Suppl. 2005 Apr;23(1):S27-33. (PMID: 15821448)
Biochim Biophys Acta. 2005 Feb 21;1687(1-3):76-83. (PMID: 15708355)
J Atheroscler Thromb. 2010 Jun 30;17(6):539-45. (PMID: 20134099)
Mol Cell Biochem. 2010 Dec;345(1-2):189-95. (PMID: 20714791)
Curr Top Med Chem. 2012;12(10):1181-91. (PMID: 22519448)
Nat Rev Cardiol. 2011 May;8(5):292-300. (PMID: 21448140)
Exp Ther Med. 2013 Sep;6(3):721-726. (PMID: 24137254)
Clin Exp Pharmacol Physiol. 2005 Sep;32(9):697-701. (PMID: 16173924)
Sci STKE. 1999 Oct 26;1999(5):RE1. (PMID: 11865184)
J Cardiovasc Pharmacol. 2006 Feb;47(2):228-35. (PMID: 16495760)
Semin Immunol. 2000 Feb;12 (1):85-98. (PMID: 10723801)
Int J Med Sci. 2011;8(7):564-72. (PMID: 21960749)
Circulation. 1999 Jun 15;99(23 ):3063-70. (PMID: 10368126)
Eur J Pharmacol. 2011 Sep;666(1-3):135-41. (PMID: 21570962)
Heart Fail Rev. 2012 Sep;17(4-5):693-706. (PMID: 21717224)
Am J Physiol Heart Circ Physiol. 2010 Mar;298(3):H1072-8. (PMID: 20081106)
Circulation. 2002 Jun 25;105(25):2937-8. (PMID: 12081982)
Neth Heart J. 2012 Jan;20(1):44-8. (PMID: 22161127)
Anesthesiology. 2013 Jun;118(6):1385-94. (PMID: 23364599)
Arq Bras Cardiol. 2010 Oct;95(5):635-9. (PMID: 20857043)
Circulation. 2001 Oct 30;104(18):2216-21. (PMID: 11684634)
Circ J. 2013;77(3):580-7. (PMID: 23358460)
Mol Biol Rep. 2011 Jun;38(5):3037-44. (PMID: 20127518)
Fundam Clin Pharmacol. 2005 Feb;19(1):117-25. (PMID: 15660968)
J Mol Cell Cardiol. 2010 Mar;48(3):445-53. (PMID: 19799912)
PLoS One. 2013;8(1):e53882. (PMID: 23349755)
Cardiovasc Res. 2004 Oct 1;64(1):24-31. (PMID: 15364610)
Exp Biol Med (Maywood). 2008 Jan;233(1):21-31. (PMID: 18156302)
Chin Med J (Engl). 2013;126(11):2149-56. (PMID: 23769575)
PLoS One. 2013 May 31;8(5):e64986. (PMID: 23741440)
PLoS One. 2015 Mar 27;10(3):e0121842. (PMID: 25816098)
J Mol Cell Cardiol. 2012 Jan;52(1):228-36. (PMID: 22119801)
Circulation. 2010 Jan 5;121(1):80-90. (PMID: 20026776)
Dev Dyn. 2004 Aug;230(4):787-94. (PMID: 15254913)
Cardiovasc Ther. 2012 Aug;30(4):e198-209. (PMID: 21884011)
Arq Bras Cardiol. 2009 Feb;92(2):150-64. (PMID: 19360249)
FASEB J. 2006 Sep;20(11):1918-20. (PMID: 16837548)
Arq Bras Cardiol. 2009 Oct;93(4):434-40, 426-32. (PMID: 19936465)
Circ Res. 2002 Mar 22;90(5):520-30. (PMID: 11909815)
Circulation. 2010 Apr 13;121(14):1645-54. (PMID: 20385961)
Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2005 Dec;149(2):225-36. (PMID: 16601761)
Arch Med Res. 2011 May;42(4):274-80. (PMID: 21820605)
Circulation. 2002 Feb 19;105(7):868-73. (PMID: 11854129)
Am J Cardiol. 2013 May 15;111(10):1394-400. (PMID: 23453459)
Physiol Rev. 2012 Apr;92(2):635-88. (PMID: 22535894)
J Mol Cell Cardiol. 2010 Mar;48(3):504-11. (PMID: 19631653)
J Mol Cell Cardiol. 2010 Mar;48(3):544-9. (PMID: 19577572)
Am J Physiol Heart Circ Physiol. 2000 Jan;278(1):H194-200. (PMID: 10644599)
J Pharm Pharm Sci. 2006;9(3):365-75. (PMID: 17207419)
Tex Heart Inst J. 2013;40(2):140-7. (PMID: 23678211)
Curr Top Med Chem. 2012;12(10):1214-21. (PMID: 22519451)
J Am Coll Cardiol. 2011 Oct 25;58(18):1833-43. (PMID: 22018293)
J Cell Sci. 2002 Oct 1;115(Pt 19):3719-27. (PMID: 12235282)
PLoS One. 2011;6(9):e25320. (PMID: 21980426)
Int J Biochem Cell Biol. 2006 Mar;38(3):358-65. (PMID: 16300990)
J Am Coll Cardiol. 2001 Aug;38(2):307-14. (PMID: 11499717)
Cardiovasc Ther. 2008 Spring;26(1):24-37. (PMID: 18466418)
Yonsei Med J. 2012 May;53(3):501-7. (PMID: 22476992)
Atherosclerosis. 1999 Dec;147(2):253-61. (PMID: 10559511)
Oncogene. 2006 Oct 30;25(51):6680-4. (PMID: 17072321)
Curr Treat Options Cardiovasc Med. 2009 Aug;11(4):339-46. (PMID: 19627666)
Heart Fail Rev. 2011 Jan;16(1):1-4. (PMID: 20872278)
Circ Cardiovasc Interv. 2012 Apr;5(2):146-9. (PMID: 22511737)
Circulation. 2000 Jun 27;101(25):2981-8. (PMID: 10869273)
Int J Inflam. 2011;2011:170352. (PMID: 21977329)
المشرفين على المادة: 0 (Anticholesteremic Agents)
0 (Interleukin-1)
0 (NF-kappa B p50 Subunit)
0 (Tissue Inhibitor of Metalloproteinase-1)
9007-34-5 (Collagen)
A0JWA85V8F (Atorvastatin)
EC 3.4.24.7 (Matrix Metalloproteinase 1)
تواريخ الأحداث: Date Created: 20161124 Date Completed: 20170627 Latest Revision: 20181202
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC5120826
DOI: 10.1371/journal.pone.0166845
PMID: 27880844
قاعدة البيانات: MEDLINE
الوصف
تدمد:1932-6203
DOI:10.1371/journal.pone.0166845