Regulation of cardiac gene expression during myocardial growth and hypertrophy: molecular studies of an adaptive physiologic response

@article{Chien1991RegulationOC,
  title={Regulation of cardiac gene expression during myocardial growth and hypertrophy: molecular studies of an adaptive physiologic response},
  author={Kenneth R Chien and Kirk U. Knowlton and Gao Zhu and Shu Chien},
  journal={The FASEB Journal},
  year={1991},
  volume={5},
  pages={3037 - 3046}
}
Studies from both in vivo and in vitro model systems have provided an initial skeleton of the potential signaling pathways that might regulate cardiac genes during growth and hypertrophy. One of the first detectable changes in cardiac gene expression is the activation of a program of immediate early gene expression, which is distinct for the hypertrophic response, and is conserved in multiple models of both in vivo and in vitro hypertrophy. Diverse and distinct hormonal stimuli have been… 
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793 Citations
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793 Citations

Expression of nuclear-acting early-response genes in the rat heart : implications for cardiac hypertrophy
TLDR
The in vivo results lend further support to the notion that the products of early-response genes structurally or functionally related to c-fos may mediate the hypertrophic actions of norepinephrine and pressure overload, which may be associated with the proliferation of cardiac non-myocyte cells which occurs concomitant with cardiac hypertrophy.
Signaling mechanisms for the activation of an embryonic gene program during the hypertrophy of cardiac ventricular muscle.
  • R. Chien
  • Biology
    Basic research in cardiology
  • 1992
TLDR
Co-transfection of a dominant negative RAS vector effectively inhibits the induction of the ANF gene during alpha adrenergic mediated hypertrophy of ventricular muscle cells, thereby establishing that a RAS-mediated pathway is required for ANF induction.
The role of protein kinases in adaptational growth of the heart.
Gene expression profiling reveals complex changes following MEK-EE expression in cardiac myocytes.
Early and transient gene expression changes in pressure overload-induced cardiac hypertrophy in mice.
Transgenic mice with cardiac-specific expression of activating transcription factor 3, a stress-inducible gene, have conduction abnormalities and contractile dysfunction.
Cellular mechanisms of cardiac hypertrophy
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A critical overview of the signalling pathways involved in the hypertrophic response is provided and a scheme to account for many of its features is provided.
Divergent transcriptional responses to independent genetic causes of cardiac hypertrophy.
TLDR
Rather than identifying a single common hypertrophic cardiomyopathy gene program, data suggest that extensive groups of genes may be useful for the prediction of specific underlying genetic determinants and condition-specific therapeutic approaches.
Mitogen-activated protein kinases mediate changes in gene expression, but not cytoskeletal organization associated with cardiac muscle cell hypertrophy
TLDR
It is found that phenylephrine treatment results in the activation of the MAP kinases and that this activity is required for transactivation of the fos, ANF, and MLH promoters, which suggests that the signal transduction pathways leading to different hypertrophic responses diverge upstream of theMAP kinases but possibly downstream of Ras.
The Role of the Transcription Factor Nuclear Factor Kappa B in the Regulation of Cardiac Hypertrophy
TLDR
Recently described mechanisms of inhibition of NF-κB activity and their application to animal models of cardiac hypertrophy are focused on and could be helpful for future studies that will be focused on the research of specific and non-toxic inhibitors of NLKB activity to regulate cardiachypertrophy and its evolution towards heart failure.
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