| Literature DB >> 27626667 |
Ines Soro-Arnaiz1, Qilong Oscar Yang Li1, Mar Torres-Capelli1, Florinda Meléndez-Rodríguez1, Sónia Veiga2, Koen Veys3, David Sebastian2, Ainara Elorza1, Daniel Tello1, Pablo Hernansanz-Agustín4, Sara Cogliati5, Jose Maria Moreno-Navarrete6, Eduardo Balsa1, Esther Fuertes1, Eduardo Romanos7, Antonio Martínez-Ruiz4, Jose Antonio Enriquez5, Jose Manuel Fernandez-Real6, Antonio Zorzano2, Katrien De Bock8, Julián Aragonés9.
Abstract
Aging is associated with progressive white adipose tissue (WAT) enlargement initiated early in life, but the molecular mechanisms involved remain unknown. Here we show that mitochondrial complex IV (CIV) activity and assembly are already repressed in white adipocytes of middle-aged mice and involve a HIF1A-dependent decline of essential CIV components such as COX5B. At the molecular level, HIF1A binds to the Cox5b proximal promoter and represses its expression. Silencing of Cox5b decreased fatty acid oxidation and promoted intracellular lipid accumulation. Moreover, local in vivo Cox5b silencing in WAT of young mice increased the size of adipocytes, whereas restoration of COX5B expression in aging mice counteracted adipocyte enlargement. An age-dependent reduction in COX5B gene expression was also found in human visceral adipose tissue. Collectively, our findings establish a pivotal role for CIV dysfunction in progressive white adipocyte enlargement during aging, which can be restored to alleviate age-dependent WAT expansion.Entities:
Keywords: COX5B; HIF-1; aging; human adipose tissue; mitochondrial complex IV; mitochondrial dysfunction; obesity; white adipocytes
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Year: 2016 PMID: 27626667 DOI: 10.1016/j.celrep.2016.08.041
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423