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Endothelial-to-mesenchymal transition contributes to cardiac fibrosis

Nature medicine, 2007-08, Vol.13 (8), p.952-961

2007

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Lack of authentic atrial fibrillation in commonly used murine atrial fibrillation models

PloS one, 2022-01, Vol.17 (1), p.e0256512-e0256512

2022

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Rapamycin attenuates load-induced cardiac hypertrophy in mice

Circulation (New York, N.Y.), 2003-04, Vol.107 (12), p.1664-1670

2003

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Gata4 Is Required for Maintenance of Postnatal Cardiac Function and Protection from Pressure Overload-Induced Heart Failure

Proceedings of the National Academy of Sciences - PNAS, 2006-09, Vol.103 (39), p.14471-14476

2006

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Deletion of Ribosomal S6 Kinases Does Not Attenuate Pathological, Physiological, or Insulin-Like Growth Factor 1 Receptor-Phosphoinositide 3-Kinase-Induced Cardiac Hypertrophy

Molecular and Cellular Biology, 2004-07, Vol.24 (14), p.6231-6240

2004

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Mouse surgical models in cardiovascular research

Methods in molecular biology (Clifton, N.J.), 2009-01, Vol.573, p.115

Tarnavski, Oleg

2009

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Haploinsufficiency of the cardiac transcription factor Nkx2-5 variably affects the expression of putative target genes

The FASEB journal, 2005-09, Vol.19 (11), p.1495-1497

2005

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Inhibition of mTOR signaling with rapamycin regresses established cardiac hypertrophy induced by pressure overload

Circulation (New York, N.Y.), 2004-06, Vol.109 (24), p.3050-3055

2004

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Correction for McMullen et al., "Deletion of Ribosomal S6 Kinases Does Not Attenuate Pathological, Physiological, or Insulin-Like Growth Factor 1 Receptor-Phosphoinositide 3-Kinase-Induced Cardiac Hypertrophy"

Molecular and cellular biology, 2021-01, Vol.41 (2)

2021

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Mouse cardiac surgery: comprehensive techniques for the generation of mouse models of human diseases and their application for genomic studies

Physiological genomics, 2004-02, Vol.16 (3), p.349-360

2004

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Transcription Factor GATA4 Is Activated but Not Required for Insulin-like Growth Factor 1 (IGF1)-induced Cardiac Hypertrophy

The Journal of biological chemistry, 2012-03, Vol.287 (13), p.9827-9834

2012

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Alterations in apoptosis regulatory factors during hypertrophy and heart failure

American journal of physiology. Heart and circulatory physiology, 2004-07, Vol.287 (1), p.H72-H80

2004

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Alterations in apoptosis regulatory factors during hypertrophy and heart failure

American journal of physiology. Heart and circulatory physiology, 2004-07, Vol.56 (1), p.H72-H80

2004

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P4-16 Comparison of gene expression in different heart regions during myocardial infarction

International journal of cardiology, 2004, Vol.97, p.S58-S58

2004

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Endothelial-to-mesenchymal transition contributes to cardiac fibrosis

Lack of authentic atrial fibrillation in commonly used murine atrial fibrillation models

Rapamycin attenuates load-induced cardiac hypertrophy in mice

Gata4 Is Required for Maintenance of Postnatal Cardiac Function and Protection from Pressure Overload-Induced Heart Failure

Deletion of Ribosomal S6 Kinases Does Not Attenuate Pathological, Physiological, or Insulin-Like Growth Factor 1 Receptor-Phosphoinositide 3-Kinase-Induced Cardiac Hypertrophy

Mouse surgical models in cardiovascular research

Haploinsufficiency of the cardiac transcription factor Nkx2-5 variably affects the expression of putative target genes

Inhibition of mTOR signaling with rapamycin regresses established cardiac hypertrophy induced by pressure overload

Correction for McMullen et al., "Deletion of Ribosomal S6 Kinases Does Not Attenuate Pathological, Physiological, or Insulin-Like Growth Factor 1 Receptor-Phosphoinositide 3-Kinase-Induced Cardiac Hypertrophy"

Mouse cardiac surgery: comprehensive techniques for the generation of mouse models of human diseases and their application for genomic studies

Transcription Factor GATA4 Is Activated but Not Required for Insulin-like Growth Factor 1 (IGF1)-induced Cardiac Hypertrophy

Alterations in apoptosis regulatory factors during hypertrophy and heart failure

Alterations in apoptosis regulatory factors during hypertrophy and heart failure

P4-16 Comparison of gene expression in different heart regions during myocardial infarction

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