Research Perspective Volume 2, Issue 12 pp 1004—1011
Opposing function of mitochondrial prohibitin in aging
- 1 Laboratory for Bioinformatics and Molecular Genetics, Bio III, Albert-Ludwigs-University of Freiburg, D-79104 Freiburg, Germany
- 2 Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology, Heraklion, 71110, Crete, Greece
received: December 14, 2010 ; accepted: December 14, 2010 ; published: December 16, 2010 ;https://doi.org/10.18632/aging.100246
How to Cite
While specific signalling cascades involved in aging, such as the insulin/IGF-1 pathway, are well-described, the actual metabolic changes they elicit to prolong lifespan remain obscure. Nevertheless, the tuning of cellular metabolism towards maximal survival is the molecular basis of longevity. The eukaryotic mitochondrial prohibitin complex is a macromolecular structure at the inner mitochondrial membrane, implicated in several important cellular processes such as mitochondrial biogenesis and function, molecular signalling, replicative senescence, and cell death. Recent studies in C. elegans have revealed that prohibitin differentially influences aging by moderating fat metabolism and energy production, in response to both intrinsic signalling events and extrinsic cues. These findings indicate that prohibitin is a context-dependent modulator of longevity. The tight evolutionary conservation and ubiquitous expression of prohibitin proteins suggest a similar role for the mitochondrial prohibitin complex during aging in other organisms.