基质金属蛋白酶在特发性肺纤维化中的作用。

Fibrogenesis & Tissue Repair Pub Date : 2012-06-06 eCollection Date: 2012-01-01 DOI:10.1186/1755-1536-5-S1-S9
Annie Pardo, Moisés Selman
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引用次数: 72

摘要

肺纤维化是多种慢性肺疾病的最终共同途径,被称为间质性肺疾病。最具侵袭性的形式是特发性肺纤维化[IPF],其特征是肺泡上皮细胞损伤/活化,成纤维细胞/肌成纤维细胞群体扩大,细胞外基质[ECM]成分过度积累,最终导致肺实质破坏。几种基质金属蛋白酶[MMPs]在IPF肺中上调,并已被证明通过细胞外基质重塑和基底膜破坏积极参与疾病的发病机制。然而,MMPs也可以分解介导细胞-细胞和细胞- ecm相互作用的分子,并可以激活生长因子和生长因子受体,这表明它们可能参与其他局部生物病理过程,如凋亡、迁移、增殖和血管生成。
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Role of matrix metaloproteases in idiopathic pulmonary fibrosis.

Lung fibrosis is the final common pathway of a large variety of chronic lung disorders, named interstitial lung diseases. The most aggressive form is the idiopathic pulmonary fibrosis [IPF] characterized by alveolar epithelial cell injury/activation, expansion of the fibroblast/myofibroblast population, and the exaggerated accumulation of extracellular matrix [ECM] components which ultimately result in the destruction of the lung parenchyma. Several matrix metalloproteases [MMPs] are upregulated in the IPF lungs and have been shown to actively participate in the pathogenesis of the disease through extracellular matrix remodeling and basement membrane disruption. However, MMPs can also breakdown molecules that mediate cell-cell and cell-ECM interactions, and can activate growth factors and growth factor receptors indicating that they likely contribute to other local biopathological processes such as apoptosis, migration, proliferation and angiogenesis.

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