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Role of mitochondrial stress and the NLRP3 inflammasome in lung diseases
BACKGROUND: As an organelle essential for intracellular energy supply, mitochondria are involved in intracellular metabolism and inflammation, and cell death. The interaction of mitochondria with the NLRP3 inflammasome in the development of lung diseases has been extensively studied. However, the ex...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer International Publishing
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10007669/ https://www.ncbi.nlm.nih.gov/pubmed/36905430 http://dx.doi.org/10.1007/s00011-023-01712-4 |
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author | Chen, Yonghu Zhang, Yuqi Li, Ning Jiang, Zhe Li, Xuezheng |
author_facet | Chen, Yonghu Zhang, Yuqi Li, Ning Jiang, Zhe Li, Xuezheng |
author_sort | Chen, Yonghu |
collection | PubMed |
description | BACKGROUND: As an organelle essential for intracellular energy supply, mitochondria are involved in intracellular metabolism and inflammation, and cell death. The interaction of mitochondria with the NLRP3 inflammasome in the development of lung diseases has been extensively studied. However, the exact mechanism by which mitochondria mediate the activation of the NLRP3 inflammasome and trigger lung disease is still unclear. METHODS: The literatures related to mitochondrial stress, NLRP3 inflammasome and lung diseases were searched in PubMed. RESULTS: This review aims to provide new insights into the recently discovered mitochondrial regulation of the NLRP3 inflammasome in lung diseases. It also describes the crucial roles of mitochondrial autophagy, long noncoding RNA, micro RNA, altered mitochondrial membrane potential, cell membrane receptors, and ion channels in mitochondrial stress and regulation of the NLRP3 inflammasome, in addition to the reduction of mitochondrial stress by nuclear factor erythroid 2-related factor 2 (Nrf2). The effective components of potential drugs for the treatment of lung diseases under this mechanism are also summarized. CONCLUSION: This review provides a resource for the discovery of new therapeutic mechanisms and suggests ideas for the development of new therapeutic drugs, thus promoting the rapid treatment of lung diseases. |
format | Online Article Text |
id | pubmed-10007669 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Springer International Publishing |
record_format | MEDLINE/PubMed |
spelling | pubmed-100076692023-03-13 Role of mitochondrial stress and the NLRP3 inflammasome in lung diseases Chen, Yonghu Zhang, Yuqi Li, Ning Jiang, Zhe Li, Xuezheng Inflamm Res Review BACKGROUND: As an organelle essential for intracellular energy supply, mitochondria are involved in intracellular metabolism and inflammation, and cell death. The interaction of mitochondria with the NLRP3 inflammasome in the development of lung diseases has been extensively studied. However, the exact mechanism by which mitochondria mediate the activation of the NLRP3 inflammasome and trigger lung disease is still unclear. METHODS: The literatures related to mitochondrial stress, NLRP3 inflammasome and lung diseases were searched in PubMed. RESULTS: This review aims to provide new insights into the recently discovered mitochondrial regulation of the NLRP3 inflammasome in lung diseases. It also describes the crucial roles of mitochondrial autophagy, long noncoding RNA, micro RNA, altered mitochondrial membrane potential, cell membrane receptors, and ion channels in mitochondrial stress and regulation of the NLRP3 inflammasome, in addition to the reduction of mitochondrial stress by nuclear factor erythroid 2-related factor 2 (Nrf2). The effective components of potential drugs for the treatment of lung diseases under this mechanism are also summarized. CONCLUSION: This review provides a resource for the discovery of new therapeutic mechanisms and suggests ideas for the development of new therapeutic drugs, thus promoting the rapid treatment of lung diseases. Springer International Publishing 2023-03-11 2023 /pmc/articles/PMC10007669/ /pubmed/36905430 http://dx.doi.org/10.1007/s00011-023-01712-4 Text en © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2023, Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic. |
spellingShingle | Review Chen, Yonghu Zhang, Yuqi Li, Ning Jiang, Zhe Li, Xuezheng Role of mitochondrial stress and the NLRP3 inflammasome in lung diseases |
title | Role of mitochondrial stress and the NLRP3 inflammasome in lung diseases |
title_full | Role of mitochondrial stress and the NLRP3 inflammasome in lung diseases |
title_fullStr | Role of mitochondrial stress and the NLRP3 inflammasome in lung diseases |
title_full_unstemmed | Role of mitochondrial stress and the NLRP3 inflammasome in lung diseases |
title_short | Role of mitochondrial stress and the NLRP3 inflammasome in lung diseases |
title_sort | role of mitochondrial stress and the nlrp3 inflammasome in lung diseases |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10007669/ https://www.ncbi.nlm.nih.gov/pubmed/36905430 http://dx.doi.org/10.1007/s00011-023-01712-4 |
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