Connective Tissue Growth Factor Overexpression in Cardiomyocytes Promotes Cardiac Hypertrophy and Protection against Pressure Overload

@article{Panek2009ConnectiveTG,
  title={Connective Tissue Growth Factor Overexpression in Cardiomyocytes Promotes Cardiac Hypertrophy and Protection against Pressure Overload},
  author={Anna N. Panek and Maximilian Georg Posch and Natalia Alenina and Santhosh Kumar Ghadge and Bettina Erdmann and Elena Popova and Andreas Perrot and Christian Geier and Rainer Dietz Ingo Morano and Michael Bader and Cemil {\"O}zcelik},
  journal={PLoS ONE},
  year={2009},
  volume={4},
  url={https://api.semanticscholar.org/CorpusID:6820215}
}
The data suggest that CTGF itself does not induce cardiac fibrosis, and is involved in hypertrophy induction and cellular remodeling depending on the cardiac stress stimulus.
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35 References

Connective tissue growth factor induces cardiac hypertrophy through Akt signaling.

Increased Connective Tissue Growth Factor Relative to Brain Natriuretic Peptide as a Determinant of Myocardial Fibrosis

Investigation of the role of connective tissue growth factor (CCN2/CTGF) and its functional interactions with brain natriuretic peptide (BNP), an antifibrotic peptide, in the development of myocardial fibrosis and diastolic heart failure suggests that a disproportionate increase in CTGF relative to BNP in cardiac myocytes plays a central role in the induction of excessive myocardia fibrosis.

Connective Tissue Growth Factor and Cardiac Fibrosis after Myocardial Infarction

There were temporal and regional differences in the expression of TGF-β1, CTGF, and collagen after MI, and the antifibrotic benefits of captopril are not mediated through a reduction in CTGF.

Induction of myocardial connective tissue growth factor in pacing-induced heart failure in pigs.

Induction of myocardial CTGF in heart failure is not just a response to ischaemia, but rather a general response to evolving heart failure.

Differential Regulation of Angiotensin II-induced Expression of Connective Tissue Growth Factor by Protein Kinase C Isoforms in the Myocardium*

It is shown that the increase in CTGF expression in cardiac tissues of streptozotocin-induced diabetic rats was reversed by captopril and islet cell transplantation and can contribute to the development of cardiac fibrosis in diabetic cardiomyopathy.

Increased expression of connective tissue growth factor in the infarct zone of experimentally induced myocardial infarction in rats.

The findings demonstrated the increased expression of CTGF in the infarct tissue after AMI was experimentally induced in rats and myocytes in theinfarct marginal zone and spindle-shaped mesenchymal cells were the cells responsible for CTGF production.

Connective tissue growth factor: a crucial cytokine-mediating cardiac fibrosis in ongoing enterovirus myocarditis

It is concluded that CTGF is a crucial molecule in the development of fibrosis in ongoing enteroviral myocarditis and downregulation of cardiac CTGF expression may open novel therapeutic approaches counteracting thedevelopment of cardiac fibrosis and subsequent heart muscle dysfunction.

Regulation of connective tissue growth factor activity in cultured rat mesangial cells and its expression in experimental diabetic glomerulosclerosis.

It is suggested that CTGF upregulation is an important factor in the pathogenesis of mesangial matrix accumulation and progressive glomerulosclerosis, acting downstream of TGF-beta.

Overexpression of connective tissue growth factor in podocytes worsens diabetic nephropathy in mice.

It is suggested that overexpression of CTGF in podocytes is sufficient to exacerbate proteinuria and mesangial expansion through a functional impairment and loss of podocytes and induction of diabetes in CTGF-transgenic mice resulted in a further elevation of endogenous CTGF mRNA expression and protein in the glomerular mesangium.

Gene regulation of connective tissue growth factor: new targets for antifibrotic therapy?