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TRIM蛋白在特发性肺纤维化中的研究进展
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Abstract:
特发性肺纤维化(IPF)是一种进行性且最终致命的纤维化肺病，可以导致进行性的肺功能下降，其发展被认为与遗传、环境、免疫、炎症、自噬、衰老等因素有关。TRIM蛋白是一个高度保守的E3泛素连接酶家族，参与多个过程：包括细胞内信号传导、发育、细胞凋亡、蛋白质质量控制、先天免疫、自噬和致癌作用，近年来，有关TRIM蛋白在疾病中的研究越来越多，研究表明它们可以参与细胞内信号传导、发育、细胞凋亡、蛋白质质量控制、先天免疫、自噬和致癌等多个过程，它们的失调会导致癌症、免疫疾病或发育障碍等疾病，参考肺纤维化所涉及的发生发展机制，TRIM蛋白在各器官纤维化中的研究也逐渐展开，本文将主要论述TRIM蛋白在肺纤维化中的研究进展。
Idiopathic pulmonary fibrosis (IPF) is a progressive and ultimately fatal fibrotic lung disease that can lead to progressive decline in lung function, and its development is thought to be related to genetic, environmental, immune, inflammatory, autophagy, aging and other factors. TRIM proteins are a highly conserved family of E3 ubiquitin ligases involved in several processes: It includes intracellular signaling, development, apoptosis, protein quality control, innate immunity, autophagy and carcinogenesis. In recent years, more and more studies on TRIM proteins in diseases have shown that they can participate in many processes such as intracellular signaling, development, apoptosis, protein quality control, innate immunity, autophagy and carcinogenesis. Their disorders can lead to cancer, immune diseases or developmental disorders and other diseases, referring to the occurrence and development mechanism involved in pulmonary fibrosis, the study of TRIM protein in various organ fibrosis is also gradually launched, this paper will mainly discuss the research progress of TRIM protein in pulmonary fibrosis.
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