Tan Jianglin, Luo Gaoxing, Wu Jun
Institute of Burn Research, State Key Laboratory for Trauma, Burns and Combined Injury, Chongqing Key Laboratory for Disease Proteomics, Southwest Hospital, Third Military Medical University Chongqing 400038, China.
Int J Burns Trauma. 2011;1(1):51-5. Epub 2011 Sep 2.
Fibrosis is the end result of pathologic wound healing and is characterized by inflammation, excessive proliferation of fibroblasts, and abnormal deposition of extracellular matrix (ECM) proteins. Despite the advanced treatments for the fibrotic diseases, as well as the researches on the fibrosis, pathologic fibrotic diseases remain to be hard cured and the molecular mechanism of fibrosis is still unclear. In our previous studies we found ITGB4BP was involved in the myofibroblast differentiation. However there were no studies about the roles of ITGB4BP in fibrosis. On this background this review explores the basic features and the biological function of ITGB4BP which might imply the underlying cellular and molecular mechanism in the regulation of fibrotic diseases.
纤维化是病理性伤口愈合的最终结果，其特征为炎症、成纤维细胞过度增殖以及细胞外基质（ECM）蛋白的异常沉积。尽管针对纤维化疾病有先进的治疗方法，且对纤维化也有诸多研究，但病理性纤维化疾病仍然难以治愈，纤维化的分子机制仍不清楚。在我们之前的研究中，我们发现整合素β4结合蛋白（ITGB4BP）参与了肌成纤维细胞的分化。然而，关于ITGB4BP在纤维化中的作用尚无相关研究。在此背景下，本综述探讨了ITGB4BP的基本特征和生物学功能，这可能暗示了纤维化疾病调控中潜在的细胞和分子机制。
