Mitochondrial (Dys) Function in Inflammaging: Do MitomiRs Influence the Energetic, Oxidative, and Inflammatory Status of Senescent Cells?

Angelica Giuliani, Francesco Prattichizzo, Luigina Micolucci, Antonio Ceriello, Antonio Domenico Procopio, Maria Rita Rippo

Research output: Contribution to journalReview article

Abstract

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.

Original languageEnglish
Pages (from-to)2309034
JournalMediators of Inflammation
Volume2017
DOIs
Publication statusPublished - 2017

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MicroRNAs
Mitochondria
Cell Aging
Phenotype
Mitochondrial Genes
Epigenomics
Inflammation

Keywords

  • Cellular Senescence
  • DNA, Mitochondrial/physiology
  • Humans
  • Inflammation/etiology
  • MicroRNAs/physiology
  • Mitochondria/physiology
  • NF-kappa B/physiology
  • Oxidative Stress
  • Reactive Oxygen Species/metabolism

Cite this

Mitochondrial (Dys) Function in Inflammaging : Do MitomiRs Influence the Energetic, Oxidative, and Inflammatory Status of Senescent Cells? / Giuliani, Angelica; Prattichizzo, Francesco; Micolucci, Luigina; Ceriello, Antonio; Procopio, Antonio Domenico; Rippo, Maria Rita.

In: Mediators of Inflammation, Vol. 2017, 2017, p. 2309034.

Research output: Contribution to journalReview article

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T2 - Do MitomiRs Influence the Energetic, Oxidative, and Inflammatory Status of Senescent Cells?

AU - Giuliani, Angelica

AU - Prattichizzo, Francesco

AU - Micolucci, Luigina

AU - Ceriello, Antonio

AU - Procopio, Antonio Domenico

AU - Rippo, Maria Rita

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N2 - 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.

AB - 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.

KW - Cellular Senescence

KW - DNA, Mitochondrial/physiology

KW - Humans

KW - Inflammation/etiology

KW - MicroRNAs/physiology

KW - Mitochondria/physiology

KW - NF-kappa B/physiology

KW - Oxidative Stress

KW - Reactive Oxygen Species/metabolism

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SN - 0962-9351

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