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Comment
. 2016 Apr 1;35(7):701-2.
doi: 10.15252/embj.201694025. Epub 2016 Feb 23.

Mitochondria and senescence: new actors for an old play

Nicolás Herranz  1 , Jesús Gil  1
Affiliations
Comment

Mitochondria and senescence: new actors for an old play

Nicolás Herranz et al. EMBO J. .

Abstract

Mitochondrial dysfunction has been linked to both cellular senescence and ageing. Despite the relationship, it is still unclear whether mitochondria have a causal role in senescence. In this issue of The EMBO Journal, Correia-Melo et al (2016) combine targeted depletion of mitochondria with impairment of their biogenesis to demonstrate that decreased numbers of mitochondria impair the senescence response. Their results suggest that targeting mitochondria could reduce the detrimental effects of senescence during ageing.

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Figures

Figure 1
Figure 1. Mitochondria are important effectors of the senescence response
Passos and colleagues (Correia‐Melo et al, 2016) describe that mitochondria form part of an autoregulatory loop involving the DNA damage response (DDR), mTOR and the production of ROS that results in persistent DDR and has a stabilizing effect on senescence.
See this image and copyright information in PMC

Comment on

  • Mitochondria are required for pro-ageing features of the senescent phenotype.
    Correia-Melo C, Marques FD, Anderson R, Hewitt G, Hewitt R, Cole J, Carroll BM, Miwa S, Birch J, Merz A, Rushton MD, Charles M, Jurk D, Tait SW, Czapiewski R, Greaves L, Nelson G, Bohlooly-Y M, Rodriguez-Cuenca S, Vidal-Puig A, Mann D, Saretzki G, Quarato G, Green DR, Adams PD, von Zglinicki T, Korolchuk VI, Passos JF. Correia-Melo C, et al. EMBO J. 2016 Apr 1;35(7):724-42. doi: 10.15252/embj.201592862. Epub 2016 Feb 4. EMBO J. 2016. PMID: 26848154 Free PMC article.

References

    1. Correia‐Melo C, Marques FD, Anderson R, Hewitt G, Hewitt R, Cole J, Carroll BM, Miwa S, Birch J, Merz A, Rushton MD, Charles M, Jurk D, Tait SW, Czapiewski R, Greaves L, Nelson G, Bohlooly‐Y M, Rodriguez‐Cuenca S, Vidal‐Puig A et al (2016) Mitochondria are required for pro‐ageing features of the senescent phenotype. EMBO J 35: 724–742 - PMC - PubMed
    1. Garcia‐Prat L, Martinez‐Vicente M, Perdiguero E, Ortet L, Rodriguez‐Ubreva J, Rebollo E, Ruiz‐Bonilla V, Gutarra S, Ballestar E, Serrano AL, Sandri M, Munoz‐Canoves P (2016) Autophagy maintains stemness by preventing senescence. Nature 529: 37–42 - PubMed
    1. Harrison DE, Strong R, Sharp ZD, Nelson JF, Astle CM, Flurkey K, Nadon NL, Wilkinson JE, Frenkel K, Carter CS, Pahor M, Javors MA, Fernandez E, Miller RA (2009) Rapamycin fed late in life extends lifespan in genetically heterogeneous mice. Nature 460: 392–395 - PMC - PubMed
    1. Herranz N, Gallage S, Mellone M, Wuestefeld T, Klotz S, Hanley CJ, Raguz S, Acosta JC, Innes AJ, Banito A, Georgilis A, Montoya A, Wolter K, Dharmalingam G, Faull P, Carroll T, Martinez‐Barbera JP, Cutillas P, Reisinger F, Heikenwalder M et al (2015) mTOR regulates MAPKAPK2 translation to control the senescence‐associated secretory phenotype. Nat Cell Biol 17: 1205–1217 - PMC - PubMed
    1. Kaplon J, Zheng L, Meissl K, Chaneton B, Selivanov VA, Mackay G, van der Burg SH, Verdegaal EM, Cascante M, Shlomi T, Gottlieb E, Peeper DS (2013) A key role for mitochondrial gatekeeper pyruvate dehydrogenase in oncogene‐induced senescence. Nature 498: 109–112 - PubMed