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

Figure 1

Potential effect of senescence-associated epigenetic rearrangement on mitochondrial function. Different damaging stimuli can induce senescence. Senescent cells bear peculiar metabolism and gene expression, which underlie a chronic proinflammatory program (SASP). This is accompanied by changes in the expression of a number of senescence-associated microRNAs (SA-miRNAs). Dysfunctional mitochondria play a major role in the promotion of the SASP. In turn, several SA-miRNAs can translocate to mitochondria (mitomiRs) and could target a plethora of mRNA with an important role within mitochondria, including transcripts derived from mitochondrial DNA (mtDNA). In this framework, we hypothesize a major role for SA-mitomiRs in determining the energetic, metabolic, and inflammatory status of senescent cells, mainly through their ability to regulate mtDNA-derived proteins.