MicroRNAs and ventricular remodeling in aortic stenosis.

[1]  I. Falcão-Pires,et al.  MicroRNAs and ventricular remodeling in aortic stenosis , 2020, Revista Portuguesa de Cardiologia (English Edition).

[2]  M. Halushka,et al.  Opportunities for microRNAs in the Crowded Field of Cardiovascular Biomarkers. , 2019, Annual review of pathology.

[3]  Qiang Liu,et al.  Transplantation of Endothelial Progenitor Cells Overexpressing miR-126-3p Improves Heart Function in Ischemic Cardiomyopathy. , 2018, Circulation journal : official journal of the Japanese Circulation Society.

[4]  V. Di Bello,et al.  MicroRNAs distribution in different phenotypes of Aortic Stenosis , 2018, Scientific Reports.

[5]  C. Rotimi,et al.  Circulating MiR-374a-5p is a potential modulator of the inflammatory process in obesity , 2018, Scientific reports.

[6]  Y. Shao,et al.  Downregulated MicroRNA-195 in the Bicuspid Aortic Valve Promotes Calcification of Valve Interstitial Cells via Targeting SMAD7 , 2017, Cellular Physiology and Biochemistry.

[7]  B. McManus,et al.  Association of Serum MiR-142-3p and MiR-101-3p Levels with Acute Cellular Rejection after Heart Transplantation , 2017, PloS one.

[8]  L. D. de Windt,et al.  miR-199b-5p is a regulator of left ventricular remodeling following myocardial infarction , 2017, Non-coding RNA research.

[9]  D. Vitantonio,et al.  Review in Translational Cardiology: MicroRNAs and Myocardial Fibrosis in Aortic Valve Stenosis, a Deep Insight on Left Ventricular Remodeling , 2016, Journal of cardiovascular echography.

[10]  J. Mariani,et al.  The transcardiac gradient of cardio‐microRNAs in the failing heart , 2016, European journal of heart failure.

[11]  Yuxiang Liu,et al.  Puerarin Attenuates Cardiac Hypertrophy Partly Through Increasing Mir-15b/195 Expression and Suppressing Non-Canonical Transforming Growth Factor Beta (Tgfβ) Signal Pathway , 2016, Medical science monitor : international medical journal of experimental and clinical research.

[12]  Douglas E. Vaughan,et al.  MiR-125b Is Critical for Fibroblast-to-Myofibroblast Transition and Cardiac Fibrosis , 2016, Circulation.

[13]  Lubo Zhang,et al.  Chronic Losartan Treatment Up-Regulates AT1R and Increases the Heart Vulnerability to Acute Onset of Ischemia and Reperfusion Injury in Male Rats , 2015, PloS one.

[14]  A. Leite-Moreira,et al.  Efeitos cardiovasculares do receptor tipo 2da angiotensina , 2014 .

[15]  I. Karakikes,et al.  Therapeutic Cardiac‐Targeted Delivery of miR‐1 Reverses Pressure Overload–Induced Cardiac Hypertrophy and Attenuates Pathological Remodeling , 2013, Journal of the American Heart Association.

[16]  R. Kalluri,et al.  Cellular mechanisms of tissue fibrosis. 1. Common and organ-specific mechanisms associated with tissue fibrosis. , 2013, American journal of physiology. Cell physiology.

[17]  A. Pasquinelli,et al.  MicroRNA biogenesis: regulating the regulators , 2013, Critical reviews in biochemistry and molecular biology.

[18]  S. Fichtlscherer,et al.  Transcoronary Concentration Gradients of Circulating MicroRNAs , 2011, Circulation.

[19]  G. Condorelli,et al.  MicroRNA-199b targets the nuclear kinase Dyrk1a in an auto-amplification loop promoting calcineurin/NFAT signalling , 2010, Nature Cell Biology.

[20]  M. Latronico,et al.  microRNAs in heart disease: putative novel therapeutic targets? , 2010, European heart journal.

[21]  Gordon K. Smyth,et al.  A comparison of background correction methods for two-colour microarrays , 2007, Bioinform..

[22]  Richard B Devereux,et al.  Recommendations for chamber quantification: a report from the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardio , 2005, Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography.

[23]  P. Carmeliet,et al.  Increased Cardiac Expression of Tissue Inhibitor of Metalloproteinase-1 and Tissue Inhibitor of Metalloproteinase-2 Is Related to Cardiac Fibrosis and Dysfunction in the Chronic Pressure-Overloaded Human Heart , 2005, Circulation.

[24]  F. Spinale Matrix metalloproteinases: regulation and dysregulation in the failing heart. , 2002, Circulation research.

[25]  C. Brilla,et al.  Lisinopril-Mediated Regression of Myocardial Fibrosis in Patients With Hypertensive Heart Disease , 2000, Circulation.

[26]  K. Weber Fibrosis and hypertensive heart disease , 2000, Current opinion in cardiology.

[27]  O. Hess,et al.  Influence of collagen network on left ventricular systolic and diastolic function in aortic valve disease. , 1993, Journal of the American College of Cardiology.

[28]  O. Hess,et al.  Diastolic dysfunction in aortic stenosis. , 1993, Circulation.

[29]  H. Schunkert,et al.  Increased rat cardiac angiotensin converting enzyme activity and mRNA expression in pressure overload left ventricular hypertrophy. Effects on coronary resistance, contractility, and relaxation. , 1990, The Journal of clinical investigation.

[30]  Mosteller Rd Simplified Calculation of Body-Surface Area , 1987 .

[31]  A. Leite-Moreira,et al.  Load independent impairment of reverse remodeling after valve replacement in hypertensive aortic stenosis patients. , 2014, International Journal of Cardiology.

[32]  J. S. Janicki,et al.  The Dynamic Interaction Between Matrix Metalloproteinase Activity and Adverse Myocardial Remodeling , 2004, Heart Failure Reviews.

[33]  I. Komuro,et al.  Gene Expression in Fibroblasts and Fibrosis: Involvement in Cardiac Hypertrophy Roles of Cardiac Transcription Factors in Cardiac Hypertrophy Ras, Akt, and Mechanotransduction in the Cardiac Myocyte G Protein–Coupled Signaling and Gene Expression Genetic Models and Mechanisms of Transcription in Car , 2003 .

[34]  R. Mosteller Simplified calculation of body-surface area. , 1987, The New England journal of medicine.