Connective tissue growth factor (CCN2, CTGF) and organ fibrosis: lessons from transgenic animals.
Connective tissue growth factor (CCN2, CTGF) and organ fibrosis: lessons from transgenic animals.
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DOI：
10.1007/s12079-009-0071-5
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发表时间：
2010-03
影响因子：
4.1
通讯作者：
Brigstock DR
中科院分区：
文献类型：
--
作者：
Brigstock DR
近几个月来，文献报道了四种不同的系统，其中CCN2转基因分别在足细胞、肝细胞、心肌细胞或呼吸上皮细胞中表达，分别在肾、肝、心或肺中实现过表达。这些转基因系统为体内CCN2对纤维化的贡献提供了有价值的信息，并开始揭示所涉及的潜在机制的复杂性。一方面，对这些动物的研究表明，CCN2过表达不一定直接导致纤维化病理，但由于其对细胞功能（如心脏）的其他影响，可能导致严重的非纤维化组织损伤。另一方面，CCN2的过度表达与发育（如肺）或纤维化损伤（如肾、肝）相关的信号通路一致，可导致纤维化的开始或加剧。这些研究的意义是在CCN2依赖性纤维化的表现需要微环境中CCN2和共刺激因子之间的相互作用的背景下讨论的。
In recent months, four different systems have been reported in the literature in which CCN2 transgenes were individually expressed in podocytes, hepatocytes, cardiomyocytes or respiratory epithelial cells to achieve overexpression in, respectively, the kidney, liver, heart, or lung. These transgenic systems have provided valuable information about the contribution of CCN2 to fibrosis in vivo and have begun to reveal the complexities of the underlying mechanisms involved. On the one hand, studies of these animals have revealed that CCN2 overexpression does not necessarily lead directly to fibrotic pathology but may cause severe non-fibrotic tissue damage due to its other effects on cell function (e.g. heart). On the other hand, overexpression of CCN2 in concert with signaling pathways associated with development (e.g. lung) or fibrosing injuries (e.g. kidney, liver) can lead to the initiation or exacerbation of fibrosis. The significance of these studies is discussed in the context of the requirement for interactions between CCN2 and co-stimulatory factors in the microenvironment for the manifestation of CCN2-dependent fibrosis.
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影响因子：
4.1
作者：
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通讯作者：
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作者：
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DOI：
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发表时间：
2009-04
影响因子：
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作者：
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通讯作者：
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影响因子：
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作者：
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通讯作者：
Brigstock, David R.