Connective tissue growth factor (CCN2, CTGF) and organ fibrosis: lessons from transgenic animals

Myofibroblast
DOI: 10.1007/s12079-009-0071-5 Publication Date: 2009-10-01T16:13:50Z
ABSTRACT
In recent months, four different systems have been reported in the literature which CCN2 transgenes were individually expressed podocytes, hepatocytes, cardiomyocytes or respiratory epithelial cells to achieve overexpression in, respectively, kidney, liver, heart, lung. These transgenic provided valuable information about contribution of fibrosis vivo and begun reveal complexities underlying mechanisms involved. On one hand, studies these animals revealed that does not necessarily lead directly fibrotic pathology but may cause severe non-fibrotic tissue damage due its other effects on cell function (e.g. heart). concert with signaling pathways associated development lung) fibrosing injuries liver) can initiation exacerbation fibrosis. The significance is discussed context requirement for interactions between co-stimulatory factors microenvironment manifestation CCN2-dependent
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