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Crosstalk between mitochondrial (dys)function and mitochondrial abundance.

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Michel, Sébastien [FUNDP] Wanet, Anaïs [FUNDP] De Pauw, Aurélia [UCL] Rommelaere, Guillaume [FUNDP] Arnould, Thierry [FUNDP] Renard, Patricia [FUNDP]

A controlled regulation of mitochondrial mass through either the production (biogenesis) or the degradation (mitochondrial quality control) of the organelle represents a crucial step for proper mitochondrial and cell function. Key steps of mitochondrial biogenesis and quality control are overviewed, with an emphasis on the role of mitochondrial chaperones and proteases that keep mitochondria fully functional, provided the mitochondrial activity impairment is not excessive. In this case, the whole organelle is degraded by mitochondrial autophagy or "mitophagy". Beside the maintenance of adequate mitochondrial abundance and functions for cell homeostasis, mitochondrial biogenesis might be enhanced, through discussed signalling pathways, in response to various physiological stimuli, like contractile activity, exposure to low temperatures, caloric restriction and stem cells differentiation. In addition, mitochondrial dysfunction might also initiate a retrograde response, enabling cell adaptation through increased mitochondrial biogenesis. Although the examples cited above suggest that the control of mitochondrial mass, through biogenesis or quality control, is beneficial to the cell/organism demands, the data generated from diverse pathologies suggest that modulations in mitochondrial abundance/functions may participate to the pathogenesis. Increased mitochondrial abundance is generally described to characterize mitochondrial myopathies as well as most cancers, and is generally accompanied by qualitative modifications of mitochondria, thereby affecting programmed cells death susceptibility. On the contrary, in ageing, obesity and type 2 diabetes, mitochondrial biogenesis and functions are generally down-regulated. The development of insulin resistance, favoured by an impaired mitochondrial function, tends to reduce the abundance of the organelle, through a vicious circle. J. Cell. Physiol. © 2011 Wiley-Liss, Inc.

Document type Article de périodique (Journal article) – Journal Article
Access type Accès restreint
Publication date 2011
Language Anglais
Journal information "Journal of Cellular Physiology" - Vol. 227, no. 6, p. 2297-310 (2012)
Peer reviewed yes
Publisher JohnWiley & Sons, Inc. ((United States) Hoboken)
issn 0021-9541
Publication status Publié
Affiliations FUNDP - SBIO_URBC (unité de recherche en biologie cellulaire)
UCL - SSS/IREC/FATH - Pôle de Pharmacologie et thérapeutique
Links
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