|1.||Wang, Nan: 7 articles (09/2015 - 01/2011)|
|2.||Zhang, Tong-Cun: 7 articles (02/2015 - 04/2006)|
|3.||Liao, Xing-Hua: 6 articles (02/2015 - 01/2011)|
|4.||Olson, Eric N: 4 articles (08/2015 - 04/2006)|
|5.||Wang, Bao-Wei: 4 articles (01/2015 - 10/2010)|
|6.||Shyu, Kou-Gi: 4 articles (01/2015 - 10/2010)|
|7.||Xu, Yong: 3 articles (07/2015 - 03/2015)|
|8.||Fang, Mingming: 3 articles (07/2015 - 03/2015)|
|9.||Miano, Joseph M: 3 articles (04/2015 - 09/2013)|
|10.||Long, Xiaochun: 3 articles (04/2015 - 09/2013)|
02/01/2014 - "Ectopic expression of myocardin further improved the therapeutic potential of BM-MSCs in a mouse model of myocardial infarction. "
10/01/2007 - "These finding indicate that in vivo myocardin gene transfer may potentially limit cardiomyocyte loss, myocardial fibrosis, and disturbances in electrical conduction caused by myocardial infarction."
09/01/2015 - "Myocardin-related transcription factor-A (MRTF-A) can transduce biomechanical and humoral signals, which can positively modulate cardiac damage induced by acute myocardial infarction (AMI). "
09/01/2015 - "Myocardin-related transcription factor-A-overexpressing bone marrow stem cells protect cardiomyocytes and alleviate cardiac damage in a rat model of acute myocardial infarction."
06/01/2015 - "To observe the impact of mesenchymal stem cells (BMSCs) transplantation on myocardial myocardin-related transcription factor-A (MRTF-A) and bcl-2 expression in rats with experimental myocardial infarction (MI). "
|2.||Vascular System Injuries
10/01/2013 - "Myocardin levels are reduced during vascular injury, in association with phenotypic switching of smooth muscle cells (SMCs). "
02/01/2014 - "Altogether, IRF8 is crucial in modulating SMC phenotype switching and neointima formation in response to vascular injury via direct interaction with the SRF/myocardin complex. "
10/01/2013 - "We show that re-expression of myocardin prevents the vascular injury response in murine carotid arteries, with reduced neointima formation due to decreased SMC migration and proliferation. "
01/01/2015 - "Overexpression of miR-145 and treatment with valsartan reversed Klf4 and myocardin protein expression induced by balloon injury and improved vascular injury. "
06/01/2013 - "Although vascular injury induced downregulation of expression of SMC differentiation markers and myocardin, a potent activator of SMC differentiation markers, repression of these markers and myocardin was attenuated in SM22α-Cre/IκBΔN mice. "
|3.||Cardiomegaly (Heart Hypertrophy)
04/06/2011 - "Our study indicates that the association of CMV IEs with myocardin-induced transcription may be involved in myocardin-mediated cardiac hypertrophy."
01/01/2011 - "Our studies indicate that besides myocardin, MRTF-A might play an important role in cardiac hypertrophy. "
09/01/2015 - "But, the effect of cooperation between PKCα and myocardin and the potential molecular mechanism by which PKCα regulates myocardin-mediated cardiac hypertrophy are unclear. "
09/01/2015 - "Myocardin plays a key role in the development of cardiac hypertrophy. "
09/19/2014 - "These results provide novel evidence that KLF4 is a regulator of cardiac hypertrophy by modulating the expression and the activity of myocardin. "
12/01/2010 - "This study was aimed to investigate the role of myocardin in hypoxia-induced phenotypic switching of rat pulmonary arterial SMCs (PASMCs). "
10/01/2010 - "In the present study, we evaluated the expression of myocardin and AngII after hypoxia in regulating gene transcription in neonatal cardiomyocytes. "
05/01/2009 - "In this study, we investigated the role of myocardin, a possible downstream effector of PKG, in SMC phenotype modulation induced by 1 and 24 h of hypoxia. "
05/01/2012 - "Cultured rat neonatal cardiomyocytes were subjected to hypoxia, and the expression of myocardin and ROS were evaluated. "
12/01/2010 - "Contribution of myocardin in the hypoxia-induced phenotypic switching of rat pulmonary arterial smooth muscle cells."
09/01/2015 - "These results demonstrated that PKCα inhibits myocardin-induced cardiomyocyte hypertrophy through the promotion of myocardin phosphorylation. "
09/01/2015 - "PKCα inhibited myocardin-induced cardiomyocyte hypertrophy, demonstrated by the decrease in cell surface area and fetal gene expression, in cardiomyocyte cells overexpressing PKCα and myocardin. "
02/15/2015 - "However, the direct role of myocardin in Ca(2+) signal-induced cardiomyocyte hypertrophy has not been explained clearly. "
02/15/2015 - "Ca²⁺ signal-induced cardiomyocyte hypertrophy through activation of myocardin."
12/01/2014 - "These data thus provide important and novel insights into the function that p65 inhibits myocardin-mediated cardiomyocyte hypertrophy by downregulating the expression and SUMO modification of myocardin and enhancing the expression of miR-1. "
|2.||Transcription Factors (Transcription Factor)
|3.||Serum Response Factor
|5.||Biological Markers (Surrogate Marker)
|9.||Messenger RNA (mRNA)
|10.||glucuronyl glucosamine glycan sulfate (Vessel)
|2.||Transplantation (Transplant Recipients)