Mitochondrial (Dys) Function in Inflammaging: Do MitomiRs Influence the Energetic, Oxidative, and Inflammatory Status of Senescent Cells?
A relevant feature of aging is chronic low-grade inflammation, termed inflammaging, a key process promoting the development of all major age-related diseases. Senescent cells can acquire the senescence-associated (SA) secretory phenotype (SASP), characterized by the secretion of proinflammatory fact...
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| Format: | Article |
| Language: | English |
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Wiley
2017-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2017/2309034 |
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| author | Angelica Giuliani Francesco Prattichizzo Luigina Micolucci Antonio Ceriello Antonio Domenico Procopio Maria Rita Rippo |
| author_facet | Angelica Giuliani Francesco Prattichizzo Luigina Micolucci Antonio Ceriello Antonio Domenico Procopio Maria Rita Rippo |
| author_sort | Angelica Giuliani |
| collection | DOAJ |
| description | A relevant feature of aging is chronic low-grade inflammation, termed inflammaging, a key process promoting the development of all major age-related diseases. Senescent cells can acquire the senescence-associated (SA) secretory phenotype (SASP), characterized by the secretion of proinflammatory factors fuelling inflammaging. Cellular senescence is also accompanied by a deep reshaping of microRNA expression and by the modulation of mitochondria activity, both master regulators of the SASP. Here, we synthesize novel findings regarding the role of mitochondria in the SASP and in the inflammaging process and propose a network linking nuclear-encoded SA-miRNAs to mitochondrial gene regulation and function in aging cells. In this conceptual structure, SA-miRNAs can translocate to mitochondria (SA-mitomiRs) and may affect the energetic, oxidative, and inflammatory status of senescent cells. We discuss the potential role of several of SA-mitomiRs (i.e., let-7b, miR-1, miR-130a-3p, miR-133a, miR-146a-5p, miR-181c-5p, and miR-378-5p), using miR-146a as a proof-of-principle model. Finally, we propose a comprehensive, metabolic, and epigenetic view of the senescence process, in order to amplify the range of possible approaches to target inflammaging, with the ultimate goal of decelerating the aging rate, postponing or blunting the development of age-related diseases. |
| format | Article |
| id | doaj-art-c4bb4055c26e4ad9b6c77f38cbf7e81e |
| institution | OA Journals |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2017-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-c4bb4055c26e4ad9b6c77f38cbf7e81e2025-08-20T02:18:46ZengWileyMediators of Inflammation0962-93511466-18612017-01-01201710.1155/2017/23090342309034Mitochondrial (Dys) Function in Inflammaging: Do MitomiRs Influence the Energetic, Oxidative, and Inflammatory Status of Senescent Cells?Angelica Giuliani0Francesco Prattichizzo1Luigina Micolucci2Antonio Ceriello3Antonio Domenico Procopio4Maria Rita Rippo5Department of Clinical and Molecular Sciences, DISCLIMO, Università Politecnica delle Marche, Ancona, ItalyIRCCS Multimedica, 20099 Sesto San Giovanni, ItalyDepartment of Clinical and Molecular Sciences, DISCLIMO, Università Politecnica delle Marche, Ancona, ItalyIRCCS Multimedica, 20099 Sesto San Giovanni, ItalyDepartment of Clinical and Molecular Sciences, DISCLIMO, Università Politecnica delle Marche, Ancona, ItalyDepartment of Clinical and Molecular Sciences, DISCLIMO, Università Politecnica delle Marche, Ancona, ItalyA relevant feature of aging is chronic low-grade inflammation, termed inflammaging, a key process promoting the development of all major age-related diseases. Senescent cells can acquire the senescence-associated (SA) secretory phenotype (SASP), characterized by the secretion of proinflammatory factors fuelling inflammaging. Cellular senescence is also accompanied by a deep reshaping of microRNA expression and by the modulation of mitochondria activity, both master regulators of the SASP. Here, we synthesize novel findings regarding the role of mitochondria in the SASP and in the inflammaging process and propose a network linking nuclear-encoded SA-miRNAs to mitochondrial gene regulation and function in aging cells. In this conceptual structure, SA-miRNAs can translocate to mitochondria (SA-mitomiRs) and may affect the energetic, oxidative, and inflammatory status of senescent cells. We discuss the potential role of several of SA-mitomiRs (i.e., let-7b, miR-1, miR-130a-3p, miR-133a, miR-146a-5p, miR-181c-5p, and miR-378-5p), using miR-146a as a proof-of-principle model. Finally, we propose a comprehensive, metabolic, and epigenetic view of the senescence process, in order to amplify the range of possible approaches to target inflammaging, with the ultimate goal of decelerating the aging rate, postponing or blunting the development of age-related diseases.http://dx.doi.org/10.1155/2017/2309034 |
| spellingShingle | Angelica Giuliani Francesco Prattichizzo Luigina Micolucci Antonio Ceriello Antonio Domenico Procopio Maria Rita Rippo Mitochondrial (Dys) Function in Inflammaging: Do MitomiRs Influence the Energetic, Oxidative, and Inflammatory Status of Senescent Cells? Mediators of Inflammation |
| title | Mitochondrial (Dys) Function in Inflammaging: Do MitomiRs Influence the Energetic, Oxidative, and Inflammatory Status of Senescent Cells? |
| title_full | Mitochondrial (Dys) Function in Inflammaging: Do MitomiRs Influence the Energetic, Oxidative, and Inflammatory Status of Senescent Cells? |
| title_fullStr | Mitochondrial (Dys) Function in Inflammaging: Do MitomiRs Influence the Energetic, Oxidative, and Inflammatory Status of Senescent Cells? |
| title_full_unstemmed | Mitochondrial (Dys) Function in Inflammaging: Do MitomiRs Influence the Energetic, Oxidative, and Inflammatory Status of Senescent Cells? |
| title_short | Mitochondrial (Dys) Function in Inflammaging: Do MitomiRs Influence the Energetic, Oxidative, and Inflammatory Status of Senescent Cells? |
| title_sort | mitochondrial dys function in inflammaging do mitomirs influence the energetic oxidative and inflammatory status of senescent cells |
| url | http://dx.doi.org/10.1155/2017/2309034 |
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