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自噬、细胞凋亡和细胞焦亡在矽肺进展中的机制及作用。

The Mechanism and Effect of Autophagy, Apoptosis, and Pyroptosis on the Progression of Silicosis.

机构信息

Key Laboratory of Molecular Epidemiology of Hunan Province, Hunan Normal University, Changsha 410013, China.

出版信息

Int J Mol Sci. 2021 Jul 28;22(15):8110. doi: 10.3390/ijms22158110.

Abstract

Silicosis remains one of the most severe pulmonary fibrotic diseases worldwide, caused by chronic exposure to silica dust. In this review, we have proposed that programmed cell death (PCD), including autophagy, apoptosis, and pyroptosis, is closely associated with silicosis progression. Furthermore, some autophagy, apoptosis, or pyroptosis-related signaling pathways or regulatory proteins have also been summarized to contribute greatly to the formation and development of silicosis. In addition, silicosis pathogenesis depends on the crosstalk among these three ways of PCD to a certain extent. In summary, more profound research on these mechanisms and effects may be expected to become promising targets for intervention or therapeutic methods of silicosis in the future.

摘要

矽肺仍然是全球最严重的肺部纤维化疾病之一,由长期暴露于硅尘引起。在这篇综述中,我们提出程序性细胞死亡(PCD),包括自噬、细胞凋亡和细胞焦亡,与矽肺的进展密切相关。此外,一些自噬、细胞凋亡或细胞焦亡相关的信号通路或调节蛋白也被总结出来,对矽肺的形成和发展有很大的贡献。此外,矽肺的发病机制在某种程度上取决于这三种 PCD 方式之间的相互作用。总之,对这些机制和作用的更深入研究可能有望成为未来矽肺干预或治疗方法的有前途的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc3f/8348676/326412d82ecd/ijms-22-08110-g001.jpg

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