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基质金属蛋白酶在特发性肺纤维化中的作用。

Role of matrix metaloproteases in idiopathic pulmonary fibrosis.

作者信息

Pardo Annie, Selman Moisés

机构信息

Facultad de Ciencias, Universidad Nacional Autónoma de México, Ciudad Universitaria, CP 04510, México DF, México ; Instituto Nacional de Enfermedades Respiratorias "Ismael Cosío Villegas", Tlalpan 4502, CP 14080, México DF, México.

出版信息

Fibrogenesis Tissue Repair. 2012 Jun 6;5(Suppl 1):S9. doi: 10.1186/1755-1536-5-S1-S9. eCollection 2012.

Abstract

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.

摘要

肺纤维化是多种慢性肺部疾病(即间质性肺疾病)的最终共同病理途径。最具侵袭性的形式是特发性肺纤维化(IPF),其特征为肺泡上皮细胞损伤/活化、成纤维细胞/肌成纤维细胞数量增加以及细胞外基质(ECM)成分过度积聚,最终导致肺实质破坏。几种基质金属蛋白酶(MMPs)在IPF肺组织中上调,并且已显示通过细胞外基质重塑和基底膜破坏而积极参与该疾病的发病机制。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,并能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,如细胞凋亡、迁移、增殖和血管生成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50da/3368759/18b742070eae/1755-1536-5-S1-S9-1.jpg

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