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Metalloproteinases in liver fibrosis: current insights

机译:肝纤维化中的金属蛋白酶:最新见解

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Liver fibrosis is defined by excessive deposition of extracellular matrix. The fibrotic conditions result from the imbalance between synthesis and deposition of fibrous tissues and decomposition of these matrix proteins. This process can be reversed as a regular part of the healing process after hepatic damage or can become chronic. When the protein matrix synthesis predominates and the decomposition is suppressed, fibrosis will progress into irreversible cirrhosis or steatosis. Among the molecular players involved in fibrotic liver diseases, metalloproteinases of matrix metalloproteinase (MMP) and a disintegrin and metalloproteinase (ADAM) families are critical in the development of liver fibrosis and its resolution. Previously, MMPs were recognized as extracellular matrix degrading enzymes. Currently, they are also known as mediators in a variety of processes related to immunity and tissue repair. In this article, we have reviewed the models of liver fibrosis and findings on MMPs and ADAMs in hepatic fibrosis conditions.
机译:肝纤维化的定义是细胞外基质过多沉积。纤维化条件是由纤维组织的合成和沉积与这些基质蛋白的分解之间的不平衡引起的。此过程可以在肝损伤后作为正常的治愈过程的一部分逆转,也可以变成慢性的。当蛋白质基质合成占主导地位并且分解受到抑制时,纤维化将发展为不可逆的肝硬化或脂肪变性。在涉及纤维化性肝病的分子参与者中,基质金属蛋白酶(MMP)的金属蛋白酶以及整联蛋白和金属蛋白酶(ADAM)家族对于肝纤维化的发展及其解决至关重要。以前,MMP被认为是细胞外基质降解酶。目前,它们在与免疫和组织修复有关的各种过程中也被称为介体。在本文中,我们回顾了肝纤维化的模型以及在肝纤维化情况下MMP和ADAM的发现。

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