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The Mechanism and Effect of Autophagy, Apoptosis, and Pyroptosis on the Progression of Silicosis
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,...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8348676/ https://www.ncbi.nlm.nih.gov/pubmed/34360876 http://dx.doi.org/10.3390/ijms22158110 |
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author | Tan, Shiyi Chen, Shi |
author_facet | Tan, Shiyi Chen, Shi |
author_sort | Tan, Shiyi |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-8348676 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-83486762021-08-08 The Mechanism and Effect of Autophagy, Apoptosis, and Pyroptosis on the Progression of Silicosis Tan, Shiyi Chen, Shi Int J Mol Sci Review 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. MDPI 2021-07-28 /pmc/articles/PMC8348676/ /pubmed/34360876 http://dx.doi.org/10.3390/ijms22158110 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Tan, Shiyi Chen, Shi The Mechanism and Effect of Autophagy, Apoptosis, and Pyroptosis on the Progression of Silicosis |
title | The Mechanism and Effect of Autophagy, Apoptosis, and Pyroptosis on the Progression of Silicosis |
title_full | The Mechanism and Effect of Autophagy, Apoptosis, and Pyroptosis on the Progression of Silicosis |
title_fullStr | The Mechanism and Effect of Autophagy, Apoptosis, and Pyroptosis on the Progression of Silicosis |
title_full_unstemmed | The Mechanism and Effect of Autophagy, Apoptosis, and Pyroptosis on the Progression of Silicosis |
title_short | The Mechanism and Effect of Autophagy, Apoptosis, and Pyroptosis on the Progression of Silicosis |
title_sort | mechanism and effect of autophagy, apoptosis, and pyroptosis on the progression of silicosis |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8348676/ https://www.ncbi.nlm.nih.gov/pubmed/34360876 http://dx.doi.org/10.3390/ijms22158110 |
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