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Mech Ageing Dev. 2017 Jul;165(Pt B):115-128. doi: 10.1016/j.mad.2016.12.002. Epub 2016 Dec 11.

Mitochondria and mitochondria-induced signalling molecules as longevity determinants.

Author information

1
Department of Biology, Ecology and Earth Science, University of Calabria, Rende (CS), Italy.
2
Department of Experimental, Diagnostic and Specialty Medicine (DIMES), University of Bologna, Via San Giacomo 12, 40126 Bologna, Italy; Interdepartmental Centre "L. Galvani" (CIG) University of Bologna, Via San Giacomo 12, 40126 Bologna, Italy. Electronic address: aurelia.santoro@unibo.it.
3
Department of Experimental, Diagnostic and Specialty Medicine (DIMES), University of Bologna, Via San Giacomo 12, 40126 Bologna, Italy; Interdepartmental Centre "L. Galvani" (CIG) University of Bologna, Via San Giacomo 12, 40126 Bologna, Italy.

Abstract

An intense cross talk between mitochondria and nucleus continuously informs the cell about the functional state of these crucial organelles and elicits an effective stress response that strenghtens the cell, promoting its survival. Interestingly, this effect can spread also in a non-cell autonomous fashion to distal tissues by means of soluble factors. This stress response is responsible of a consistent lifespan increase in many animal models, while in humans there is still a lack of knowledge. This review summarises the available data on the involvement of mitochondria in longevity focusing in particular on this signalling activity and the consequent stress response that is elicited, and proposes the idea that, similarly to animal models, humans may benefit from this response in terms of delayed aging and longevity.

KEYWORDS:

Human longevity; Mito-nuclear communication; Mitochondria; Mitochondrial epigenetics; Mitochondrial uncoupling; Mitokines; UPR(mt)

PMID:
27964991
DOI:
10.1016/j.mad.2016.12.002
[Indexed for MEDLINE]

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