自噬在肺纤维化中的作用机制

The Mechanism of Autophagy in Pulmonary Fibrosis

自噬是一个高度保守的细胞降解和循环过程,是维持细胞器和细胞蛋白质合成、降解和再循环之间稳态平衡的重要因素。自噬是一种细胞保护机制,其功能障碍涉及许多疾病,包括特发性肺纤维化,但目前其发病机制尚不明确。肺纤维化早期以反复微损伤导致纤维化环境,后期因成纤维细胞大量增殖、细胞外基质沉积导致肺结构及功能破坏,从而发展为不可逆的肺纤维化。在肺纤维化中,自噬不足可导致成纤维细胞活化、肌成纤维细胞分化和细胞外基质沉积,这对于肺纤维化研究有重要意义。因此,未来深入探讨自噬在肺纤维化中的发生发展机制,可为肺纤维化的诊断和治疗提供新思路。

Autophagy is a highly conserved process of cell degradation and circulation that is an important factor in maintaining organelle and homeostasis between cellular protein synthesis,degradation and recycling.Autophagy is a cellular protective mechanism,and its dysfunction involves many diseases,including idiopathic pulmonary fibrosis,but the pathogenesis still remains unclear.In the early stage of pulmonary fibrosis,repeated micro-injury leads to fibrosis environment,and in the later stage fibroblast proliferation and extracellular matrix deposition lead to the destruction of lung structure and function,which leads to the development of irreversible pulmonary fibrosis.In pulmonary fibrosis,inadequate autophagy can lead to fibroblast activation,myofibroblast differentiation and extracellular matrix deposition,which is of great significance for the study of pulmonary fibrosis.Therefore,further study on the mechanism of autophagy in pulmonary fibrosis in the future can provide new ideas for the diagnosis and treatment.