Cell Death and Inflammation: The Role of Mitochondria in Health and Disease
Mitochondria serve as a hub for a multitude of vital cellular processes. To ensure an efficient deployment of mitochondrial tasks, organelle homeostasis needs to be preserved. Mitochondrial quality control (MQC) mechanisms (i.e., mitochondrial dynamics, biogenesis, proteostasis, and autophagy) are i...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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MDPI AG
2021-03-01
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| Series: | Cells |
| Subjects: | |
| Online Access: | https://www.mdpi.com/2073-4409/10/3/537 |
| _version_ | 1827603656839528448 |
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| author | Anna Picca Riccardo Calvani Hélio José Coelho-Junior Emanuele Marzetti |
| author_facet | Anna Picca Riccardo Calvani Hélio José Coelho-Junior Emanuele Marzetti |
| author_sort | Anna Picca |
| collection | DOAJ |
| description | Mitochondria serve as a hub for a multitude of vital cellular processes. To ensure an efficient deployment of mitochondrial tasks, organelle homeostasis needs to be preserved. Mitochondrial quality control (MQC) mechanisms (i.e., mitochondrial dynamics, biogenesis, proteostasis, and autophagy) are in place to safeguard organelle integrity and functionality. Defective MQC has been reported in several conditions characterized by chronic low-grade inflammation. In this context, the displacement of mitochondrial components, including mitochondrial DNA (mtDNA), into the extracellular compartment is a possible factor eliciting an innate immune response. The presence of bacterial-like CpG islands in mtDNA makes this molecule recognized as a damaged-associated molecular pattern by the innate immune system. Following cell death-triggering stressors, mtDNA can be released from the cell and ignite inflammation via several pathways. Crosstalk between autophagy and apoptosis has emerged as a pivotal factor for the regulation of mtDNA release, cell’s fate, and inflammation. The repression of mtDNA-mediated interferon production, a powerful driver of immunological cell death, is also regulated by autophagy–apoptosis crosstalk. Interferon production during mtDNA-mediated inflammation may be exploited for the elimination of dying cells and their conversion into elements driving anti-tumor immunity. |
| first_indexed | 2024-03-09T05:43:48Z |
| format | Article |
| id | doaj.art-0c4abbcd0a3d454e915699187624e2fb |
| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-09T05:43:48Z |
| publishDate | 2021-03-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cells |
| spelling | doaj.art-0c4abbcd0a3d454e915699187624e2fb2023-12-03T12:22:51ZengMDPI AGCells2073-44092021-03-0110353710.3390/cells10030537Cell Death and Inflammation: The Role of Mitochondria in Health and DiseaseAnna Picca0Riccardo Calvani1Hélio José Coelho-Junior2Emanuele Marzetti3Fondazione Policlinico Universitario “Agostino Gemelli” IRCCS, 00168 Rome, ItalyFondazione Policlinico Universitario “Agostino Gemelli” IRCCS, 00168 Rome, ItalyUniversità Cattolica del Sacro Cuore, Institute of Internal Medicine and Geriatrics, 00168 Rome, ItalyFondazione Policlinico Universitario “Agostino Gemelli” IRCCS, 00168 Rome, ItalyMitochondria serve as a hub for a multitude of vital cellular processes. To ensure an efficient deployment of mitochondrial tasks, organelle homeostasis needs to be preserved. Mitochondrial quality control (MQC) mechanisms (i.e., mitochondrial dynamics, biogenesis, proteostasis, and autophagy) are in place to safeguard organelle integrity and functionality. Defective MQC has been reported in several conditions characterized by chronic low-grade inflammation. In this context, the displacement of mitochondrial components, including mitochondrial DNA (mtDNA), into the extracellular compartment is a possible factor eliciting an innate immune response. The presence of bacterial-like CpG islands in mtDNA makes this molecule recognized as a damaged-associated molecular pattern by the innate immune system. Following cell death-triggering stressors, mtDNA can be released from the cell and ignite inflammation via several pathways. Crosstalk between autophagy and apoptosis has emerged as a pivotal factor for the regulation of mtDNA release, cell’s fate, and inflammation. The repression of mtDNA-mediated interferon production, a powerful driver of immunological cell death, is also regulated by autophagy–apoptosis crosstalk. Interferon production during mtDNA-mediated inflammation may be exploited for the elimination of dying cells and their conversion into elements driving anti-tumor immunity.https://www.mdpi.com/2073-4409/10/3/537apoptosisdamage-associated molecular patterns (DAMPs)immunogenic cell deathinnate immunitymitochondrial dysfunctionmitophagy |
| spellingShingle | Anna Picca Riccardo Calvani Hélio José Coelho-Junior Emanuele Marzetti Cell Death and Inflammation: The Role of Mitochondria in Health and Disease Cells apoptosis damage-associated molecular patterns (DAMPs) immunogenic cell death innate immunity mitochondrial dysfunction mitophagy |
| title | Cell Death and Inflammation: The Role of Mitochondria in Health and Disease |
| title_full | Cell Death and Inflammation: The Role of Mitochondria in Health and Disease |
| title_fullStr | Cell Death and Inflammation: The Role of Mitochondria in Health and Disease |
| title_full_unstemmed | Cell Death and Inflammation: The Role of Mitochondria in Health and Disease |
| title_short | Cell Death and Inflammation: The Role of Mitochondria in Health and Disease |
| title_sort | cell death and inflammation the role of mitochondria in health and disease |
| topic | apoptosis damage-associated molecular patterns (DAMPs) immunogenic cell death innate immunity mitochondrial dysfunction mitophagy |
| url | https://www.mdpi.com/2073-4409/10/3/537 |
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